Entity Extraction Examples (1854)

check_circle_outline   F1 = 100.000
check_circle_outline   F1 >= 50.00
highlight_off   F1 < 50.00
  True Positive  
  False Positive  
  False Negative

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2.4018 40.9627 10.1647 There is a single DNAmethionine codon-initiated open reading frame of 1,458 nt in frame with a homeobox and a CAX repeat , and the open reading frame is predicted to encode a protein of 51,659 daltons.
2.1632 30.9109 10.1215 There is a single methionine codon-initiated open reading frame of 1,458 nt in frame with a homeobox and a CAX repeat , and the DNAopen reading frame is predicted to encode a protein of 51,659 daltons.
0.8242 1.0000 1.0000 There is a single methionine codon-initiated open reading frame of 1,458 nt in frame with a DNAhomeobox and a CAX repeat , and the open reading frame is predicted to encode a protein of 51,659 daltons.
0.6974 0.9971 1.0000 There is a single methionine codon-initiated open reading frame of 1,458 nt in frame with a homeobox and a DNACAX repeat , and the open reading frame is predicted to encode a protein of 51,659 daltons.
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0.9248 1.0000 1.0000 When the homeodomain from DNAHB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged Drosophila homeodomain , H2.0, it was found to be 80% identical.
1.5614 10.5099 1.0000 When the homeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged proteinDrosophila homeodomain , H2.0, it was found to be 80% identical.
1.3126 20.0225 1.0000 When the proteinhomeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged Drosophila homeodomain , H2.0, it was found to be 80% identical.
0.8890 1.0000 1.0000 When the homeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged Drosophila proteinhomeodomain , H2.0, it was found to be 80% identical.
When the homeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged Drosophila DNAhomeodomain , H2.0, it was found to be 80% identical.
When the DNAhomeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged Drosophila homeodomain , H2.0, it was found to be 80% identical.
When the homeodomain from HB24 was compared to known mammalian and Drosophila homeodomains it was found to be only moderately conserved, but when it was compared to a highly diverged DNADrosophila homeodomain , H2.0, it was found to be 80% identical.
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2.6931 20.5372 1.0000 The HB24 mRNA was absent or present at low levels in normal B and T lymphocytes ; however, with the appropriate activation signal RNAHB24 mRNA was induced within several hours even in the presence of cycloheximide .
1.8103 10.7270 1.0000 The RNAHB24 mRNA was absent or present at low levels in normal B and T lymphocytes ; however, with the appropriate activation signal HB24 mRNA was induced within several hours even in the presence of cycloheximide .
2.0372 20.7163 0.9932 The HB24 mRNA was absent or present at low levels in normal B and T lymphocytes ; however, with the appropriate activation signal DNAHB24 mRNA was induced within several hours even in the presence of cycloheximide .
1.5236 10.8909 0.9863 The DNAHB24 mRNA was absent or present at low levels in normal B and T lymphocytes ; however, with the appropriate activation signal HB24 mRNA was induced within several hours even in the presence of cycloheximide .
The HB24 mRNA was absent or present at low levels in normal B and cell_typeT lymphocytes ; however, with the appropriate activation signal HB24 mRNA was induced within several hours even in the presence of cycloheximide .
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1.7200 10.8804 1.0000 Characterization of DNAHB24 expression in lymphoid and select developing tissues was performed by in situ hybridization .
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1.7672 10.0935 1.0000 HB24 is likely to have an important role in cell_typelymphocytes as well as in certain developing tissues .
0.9486 1.0000 1.0000 DNAHB24 is likely to have an important role in lymphocytes as well as in certain developing tissues .
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4.0552 30.3046 10.9835 Platelet-activating factor induces phospholipid turnover , calcium flux , arachidonic acid liberation , eicosanoid generation , and oncogene expression in a cell_linehuman B cell line .
0.9013 0.9998 1.0000 proteinPlatelet-activating factor induces phospholipid turnover , calcium flux , arachidonic acid liberation , eicosanoid generation , and oncogene expression in a human B cell line .
Platelet-activating factor induces phospholipid turnover , calcium flux , arachidonic acid liberation , eicosanoid generation , and DNAoncogene expression in a human B cell line .
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0.8916 0.9999 0.9999 proteinPlatelet-activating factor is a potent mediator of the inflammatory response .
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2.0820 20.7758 1.0000 Studies of the actions of proteinplatelet-activating factor have centered mainly around neutrophils , monocytes , and platelets .
1.6166 10.9218 0.9999 Studies of the actions of platelet-activating factor have centered mainly around neutrophils , monocytes , and cell_typeplatelets .
1.5320 10.7247 1.0000 Studies of the actions of platelet-activating factor have centered mainly around cell_typeneutrophils , monocytes , and platelets .
0.9047 1.0000 1.0000 Studies of the actions of platelet-activating factor have centered mainly around neutrophils , cell_typemonocytes , and platelets .
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2.1855 20.6277 0.9999 In this report we begin to uncover the influence of proteinplatelet-activating factor on B lymphocytes .
1.4720 10.8983 0.9997 In this report we begin to uncover the influence of platelet-activating factor on cell_typeB lymphocytes .
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4.8101 20.6781 20.3450 Employing the cell_lineEBV-transformed human B cell line SKW6.4 , we demonstrate that platelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10(-9) to 10(-6) M.
2.2562 20.4319 1.0000 Employing the EBV-transformed human B cell line SKW6.4 , we demonstrate that proteinplatelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10(-9) to 10(-6) M.
0.9459 0.9984 0.9999 Employing the EBV-transformed human B cell line cell_lineSKW6.4 , we demonstrate that platelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10(-9) to 10(-6) M.
2.6040 20.7617 20.3573 Employing the cell_lineEBV-transformed human B cell line SKW6.4 , we demonstrate that platelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10(-9) to 10(-6) M.
Employing the EBV-transformed cell_linehuman B cell line SKW6.4 , we demonstrate that platelet-activating factor significantly alters membrane phospholipid metabolism indicated by the incorporation of 32P into phosphatidylcholine , phosphatidylinositol , and phosphatidic acid but not significantly into phosphatidylethanolamine at concentrations ranging from 10(-9) to 10(-6) M.
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1.7255 10.7714 1.0000 The inactive precursor, proteinlyso-platelet-activating factor , at a concentration as high as 10(-7) M had no effect on any of the membrane phospholipids .
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2.3857 20.4854 1.0000 We also show that proteinplatelet-activating factor from 10(-12) to 10(-6) M induced rapid and significant elevation in intracellular calcium levels , whereas lyso- platelet-activating factor was again ineffective.
1.3485 20.2716 10.1085 We also show that platelet-activating factor from 10(-12) to 10(-6) M induced rapid and significant elevation in intracellular calcium levels , whereas lyso- proteinplatelet-activating factor was again ineffective.
2.3881 20.5147 10.6097 We also show that platelet-activating factor from 10(-12) to 10(-6) M induced rapid and significant elevation in intracellular calcium levels , whereas proteinlyso- platelet-activating factor was again ineffective.
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2.3281 20.3536 1.0000 We further demonstrate the impact of proteinplatelet-activating factor binding to B cells by measuring platelet-activating factor induced arachidonic acid release and 5-hydroxyeicosatetraenoic acid production.
1.6211 10.9622 1.0000 We further demonstrate the impact of platelet-activating factor binding to B cells by measuring proteinplatelet-activating factor induced arachidonic acid release and 5-hydroxyeicosatetraenoic acid production.
1.5653 10.9136 0.9999 We further demonstrate the impact of platelet-activating factor binding to cell_typeB cells by measuring platelet-activating factor induced arachidonic acid release and 5-hydroxyeicosatetraenoic acid production.
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2.0642 20.0928 0.9991 Moreover, platelet-activating factor was capable of inducing transcription of the DNAnuclear proto-oncogenes c-fos and c-jun .
1.5120 10.0648 0.9999 Moreover, proteinplatelet-activating factor was capable of inducing transcription of the nuclear proto-oncogenes c-fos and c-jun .
0.9378 1.0000 1.0000 Moreover, platelet-activating factor was capable of inducing transcription of the nuclear proto-oncogenes DNAc-fos and c-jun .
0.9343 1.0000 1.0000 Moreover, platelet-activating factor was capable of inducing transcription of the nuclear proto-oncogenes c-fos and DNAc-jun .
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2.3805 20.3991 1.0000 Finally we explored the possible role of 5-hydroxyeicosatetraenoic acid as a regulator of arachidonic acid liberation demonstrating that endogenous 5-lipoxygenase activity modulates platelet-activating factor induced arachidonic acid release perhaps acting at the level of proteinphospholipase A2 .
1.6588 10.7170 1.0000 Finally we explored the possible role of 5-hydroxyeicosatetraenoic acid as a regulator of arachidonic acid liberation demonstrating that endogenous 5-lipoxygenase activity modulates proteinplatelet-activating factor induced arachidonic acid release perhaps acting at the level of phospholipase A2 .
0.9639 1.0000 1.0000 Finally we explored the possible role of 5-hydroxyeicosatetraenoic acid as a regulator of arachidonic acid liberation demonstrating that endogenous protein5-lipoxygenase activity modulates platelet-activating factor induced arachidonic acid release perhaps acting at the level of phospholipase A2 .
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3.9790 20.9323 10.9186 In summary, platelet-activating factor is shown here to have a direct and profound effect on a cell_linepure B cell line .
1.4388 20.7154 1.0000 In summary, proteinplatelet-activating factor is shown here to have a direct and profound effect on a pure B cell line .
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3.6305 20.3866 10.8206 Positive and negative regulation of immunoglobulin gene expression by a novel DNAB-cell-specific enhancer element .
2.0649 20.1787 0.9999 Positive and negative regulation of DNAimmunoglobulin gene expression by a novel B-cell-specific enhancer element .
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5.4193 30.2162 10.9242 A new B-cell-specific enhancer element has been identified 3' of E4 and the octamerlike motifs in the DNAhuman immunoglobulin heavy-chain gene enhancer .
3.3985 20.4050 10.6894 A new DNAB-cell-specific enhancer element has been identified 3' of E4 and the octamerlike motifs in the human immunoglobulin heavy-chain gene enhancer .
1.1691 10.6093 0.9998 A new B-cell-specific enhancer element has been identified 3' of E4 and the DNAoctamerlike motifs in the human immunoglobulin heavy-chain gene enhancer .
0.8504 0.9999 1.0000 A new B-cell-specific enhancer element has been identified 3' of DNAE4 and the octamerlike motifs in the human immunoglobulin heavy-chain gene enhancer .
A new B-cell-specific enhancer element has been identified 3' of E4 and the octamerlike motifs in the proteinhuman immunoglobulin heavy-chain gene enhancer .
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4.1641 20.7167 10.8267 Tandem copies of this 67-bp MnlI-AluI fragment , when fused to the chloramphenicol acetyltransferase gene driven by the conalbumin promoter , stimulated transcription in B cells but not in cell_lineJurkat T cells or HeLa cells .
3.8577 20.8639 10.3298 Tandem copies of this DNA67-bp MnlI-AluI fragment , when fused to the chloramphenicol acetyltransferase gene driven by the conalbumin promoter , stimulated transcription in B cells but not in Jurkat T cells or HeLa cells .
2.8969 20.8240 10.1505 Tandem copies of this 67-bp MnlI-AluI fragment , when fused to the DNAchloramphenicol acetyltransferase gene driven by the conalbumin promoter , stimulated transcription in B cells but not in Jurkat T cells or HeLa cells .
2.1089 20.1042 0.9999 Tandem copies of this 67-bp MnlI-AluI fragment , when fused to the chloramphenicol acetyltransferase gene driven by the conalbumin promoter , stimulated transcription in cell_typeB cells but not in Jurkat T cells or HeLa cells .
2.0627 20.0917 0.9999 Tandem copies of this 67-bp MnlI-AluI fragment , when fused to the chloramphenicol acetyltransferase gene driven by the DNAconalbumin promoter , stimulated transcription in B cells but not in Jurkat T cells or HeLa cells .
1.5175 10.3723 0.9992 Tandem copies of this 67-bp MnlI-AluI fragment , when fused to the chloramphenicol acetyltransferase gene driven by the conalbumin promoter , stimulated transcription in B cells but not in Jurkat T cells or cell_lineHeLa cells .
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2.2404 20.0671 0.9999 Footprinting analysis revealed that the identical sequence CCGAAACTGAAAAGG , designated E6 , was protected by nuclear extracts from cell_typeB cells , T cells , or HeLa cells.
1.7514 10.2843 1.0000 Footprinting analysis revealed that the identical sequence CCGAAACTGAAAAGG , designated DNAE6 , was protected by nuclear extracts from B cells , T cells , or HeLa cells.
1.6300 10.4547 0.9999 Footprinting analysis revealed that the identical sequence CCGAAACTGAAAAGG , designated E6 , was protected by nuclear extracts from B cells , cell_typeT cells , or HeLa cells.
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1.5181 10.7551 0.9994 Gel mobility shift assays using a synthetic E6 motif detected a B-cell-specific complex in addition to a ubiquitous band found also in T cells and cell_lineHeLa cells .
1.4252 10.8544 0.9999 Gel mobility shift assays using a synthetic E6 motif detected a proteinB-cell-specific complex in addition to a ubiquitous band found also in T cells and HeLa cells .
1.3975 10.7839 0.9998 Gel mobility shift assays using a synthetic E6 motif detected a B-cell-specific complex in addition to a ubiquitous band found also in cell_typeT cells and HeLa cells .
2.1061 20.1133 1.0000 Gel mobility shift assays using a synthetic E6 motif detected a B-cell-specific complex in addition to a proteinubiquitous band found also in T cells and HeLa cells .
2.0576 20.0127 0.9999 Gel mobility shift assays using a synthetic DNAE6 motif detected a B-cell-specific complex in addition to a ubiquitous band found also in T cells and HeLa cells .
1.6682 10.1110 0.9684 Gel mobility shift assays using a synthetic DNAE6 motif detected a B-cell-specific complex in addition to a ubiquitous band found also in T cells and HeLa cells .
Gel mobility shift assays using a DNAsynthetic E6 motif detected a B-cell-specific complex in addition to a ubiquitous band found also in T cells and HeLa cells .
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2.3041 20.8358 1.0000 In agreement with the results of gel retardation assays , tandem copies of the DNAE6 motif stimulated transcription in ARH77 and Raji cells but not in Jurkat or HeLa cells .
1.7933 10.0771 1.0000 In agreement with the results of gel retardation assays , tandem copies of the E6 motif stimulated transcription in cell_lineARH77 and Raji cells but not in Jurkat or HeLa cells .
1.7176 10.1674 1.0000 In agreement with the results of gel retardation assays , tandem copies of the E6 motif stimulated transcription in ARH77 and Raji cells but not in cell_lineJurkat or HeLa cells .
1.5696 10.1995 0.9999 In agreement with the results of gel retardation assays , tandem copies of the E6 motif stimulated transcription in ARH77 and cell_lineRaji cells but not in Jurkat or HeLa cells .
1.5349 10.4348 0.9996 In agreement with the results of gel retardation assays , tandem copies of the E6 motif stimulated transcription in ARH77 and Raji cells but not in Jurkat or cell_lineHeLa cells .
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3.1151 20.2880 10.5402 Furthermore, a DNAmutant E6 motif lost both in vitro binding activity and in vivo enhancer activity .
0.6869 0.9995 0.9997 Furthermore, a mutant DNAE6 motif lost both in vitro binding activity and in vivo enhancer activity .
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3.9701 20.9424 10.9337 In striking contrast to the DNAmouse Ig heavy-chain enhancer , in which the octamer motif acts as a B-cell-specific enhancer element , the human enhancer contains an octamerlike sequence with one base substitution which bound octamer-binding proteins with only very low affinity and showed no enhancer activity of its own.
3.5042 20.7802 10.4745 In striking contrast to the mouse Ig heavy-chain enhancer , in which the octamer motif acts as a DNAB-cell-specific enhancer element , the human enhancer contains an octamerlike sequence with one base substitution which bound octamer-binding proteins with only very low affinity and showed no enhancer activity of its own.
2.2313 20.6892 1.0000 In striking contrast to the mouse Ig heavy-chain enhancer , in which the octamer motif acts as a B-cell-specific enhancer element , the human enhancer contains an octamerlike sequence with one base substitution which bound proteinoctamer-binding proteins with only very low affinity and showed no enhancer activity of its own.
2.1503 20.3578 0.9999 In striking contrast to the mouse Ig heavy-chain enhancer , in which the octamer motif acts as a B-cell-specific enhancer element , the DNAhuman enhancer contains an octamerlike sequence with one base substitution which bound octamer-binding proteins with only very low affinity and showed no enhancer activity of its own.
2.1204 20.0778 0.9999 In striking contrast to the mouse Ig heavy-chain enhancer , in which the DNAoctamer motif acts as a B-cell-specific enhancer element , the human enhancer contains an octamerlike sequence with one base substitution which bound octamer-binding proteins with only very low affinity and showed no enhancer activity of its own.
2.0856 20.3407 0.9999 In striking contrast to the mouse Ig heavy-chain enhancer , in which the octamer motif acts as a B-cell-specific enhancer element , the human enhancer contains an DNAoctamerlike sequence with one base substitution which bound octamer-binding proteins with only very low affinity and showed no enhancer activity of its own.
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1.6132 10.0453 1.0000 Interestingly, the MnlI-AluI fragment could suppress the basal-level activity of the conalbumin promoter in both cell_lineJurkat and HeLa cells .
1.4704 10.6531 0.9999 Interestingly, the DNAMnlI-AluI fragment could suppress the basal-level activity of the conalbumin promoter in both Jurkat and HeLa cells .
1.4387 10.9265 0.9999 Interestingly, the MnlI-AluI fragment could suppress the basal-level activity of the DNAconalbumin promoter in both Jurkat and HeLa cells .
0.7627 0.9984 0.9997 Interestingly, the MnlI-AluI fragment could suppress the basal-level activity of the conalbumin promoter in both Jurkat and cell_lineHeLa cells .
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2.0553 20.8319 0.9999 Moreover, simian virus 40 enhancer activity was blocked by the DNAMnlI-AluI fragment in HeLa cells but not in B cells .
2.0359 20.7502 0.9996 Moreover, simian virus 40 enhancer activity was blocked by the MnlI-AluI fragment in HeLa cells but not in cell_typeB cells .
1.4160 10.9928 0.9999 Moreover, simian virus 40 enhancer activity was blocked by the MnlI-AluI fragment in cell_lineHeLa cells but not in B cells .
2.9631 10.6893 10.1382 Moreover, DNAsimian virus 40 enhancer activity was blocked by the MnlI-AluI fragment in HeLa cells but not in B cells .
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0.8439 0.9989 0.9999 Thus, the novel enhancer element identified in this study is probably a target site for both positive and proteinnegative factors .
0.5514 1.0000 0.9990 Thus, the novel enhancer element identified in this study is probably a target site for both proteinpositive and negative factors .
4.4559 20.2425 10.7260 Thus, the DNAnovel enhancer element identified in this study is probably a target site for both positive and negative factors .
1.2473 10.4496 0.9999 Thus, the novel enhancer element identified in this study is probably a DNAtarget site for both positive and negative factors .
Thus, the novel enhancer element identified in this study is probably a target site for both proteinpositive and negative factors .
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2.5881 20.6576 1.0000 The involvement of proteinion channels in B and T lymphocyte activation is supported by many reports of changes in ion fluxes and membrane potential after mitogen binding .
1.8043 10.3166 1.0000 The involvement of ion channels in B and T lymphocyte activation is supported by many reports of changes in ion fluxes and membrane potential after proteinmitogen binding .
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4.0565 20.6297 10.9221 We have used charybdotoxin , a known inhibitor of proteinCa(2+)-dependent K+ channels , to study the role of these channels in lymphocyte activation and mitogenesis .
0.9360 1.0000 1.0000 We have used charybdotoxin , a known inhibitor of Ca(2+)-dependent K+ channels , to study the role of these channels in cell_typelymphocyte activation and mitogenesis .
0.5143 0.9998 0.9998 We have used charybdotoxin , a known inhibitor of Ca(2+)-dependent proteinK+ channels , to study the role of these channels in lymphocyte activation and mitogenesis .
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3.9717 20.6648 10.8402 However, blockade of the proteinCa(2+)-activated K+ channel is not associated with changes in cell-cycle gene activation , IL-2 production , IL-2R expression or B and T cell mitogenesis .
1.7298 10.2450 1.0000 However, blockade of the Ca(2+)-activated K+ channel is not associated with changes in cell-cycle gene activation , IL-2 production , proteinIL-2R expression or B and T cell mitogenesis .
1.7295 10.0805 1.0000 However, blockade of the Ca(2+)-activated K+ channel is not associated with changes in cell-cycle gene activation , proteinIL-2 production , IL-2R expression or B and T cell mitogenesis .
1.5317 10.9471 0.9999 However, blockade of the Ca(2+)-activated K+ channel is not associated with changes in DNAcell-cycle gene activation , IL-2 production , IL-2R expression or B and T cell mitogenesis .
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4.1495 20.8902 10.8269 These results imply that membrane potential changes secondary to the ligand-dependent opening of proteinCa(2+)-activated K+ channels are not involved in B and T lymphocyte activation and mitogenesis .
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4.3454 20.3701 10.9900 Activity of the kappa B enhancer of the proteininterleukin-2 receptor alpha chain in somatic cell hybrids is accompanied by the nuclear localization of NF-kappa B .
3.9286 20.6014 10.9218 Activity of the DNAkappa B enhancer of the interleukin-2 receptor alpha chain in somatic cell hybrids is accompanied by the nuclear localization of NF-kappa B .
2.9113 20.4841 10.8978 Activity of the kappa B enhancer of the interleukin-2 receptor alpha chain in cell_linesomatic cell hybrids is accompanied by the nuclear localization of NF-kappa B .
2.0324 20.1674 0.9999 Activity of the kappa B enhancer of the interleukin-2 receptor alpha chain in somatic cell hybrids is accompanied by the nuclear localization of proteinNF-kappa B .
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2.0141 20.5160 1.0000 The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the proteinDNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
1.6254 10.0588 1.0000 The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called proteinKBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
1.5381 10.5478 1.0000 The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of proteinNF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
0.9774 1.0000 1.0000 The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( proteinp50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
0.9497 1.0000 1.0000 The two nuclear proteins NF-kappa B (consisting of subunits p50 an proteindp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
0.9369 1.0000 1.0000 The two nuclear proteins NF-kappa B (consisting of subunits proteinp50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
0.8768 0.9969 1.0000 The two nuclear proteins proteinNF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
5.6613 30.9199 20.7959 The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the cell_linehuman T-cell line IARC 301.5 .
1.9614 20.2304 0.9994 The two proteinnuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line cell_lineIARC 301.5 .
The proteintwo nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the human T-cell line IARC 301.5 .
The two nuclear proteins NF-kappa B (consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa B ( p50 ) by itself, also called KBF1 , are constitutively expressed and localized in the nucleus of the cell_linehuman T-cell line IARC 301.5 .
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3.6644 20.8165 10.5870 In order to define the roles of these two factors , which bind to the same DNAkappa B enhancers , in transcription activation we have prepared somatic cell hybrids between IARC 301.5 and a murine myeloma .
1.6590 10.5823 0.9999 In order to define the roles of these two factors , which bind to the same kappa B enhancers , in transcription activation we have prepared somatic cell hybrids between cell_lineIARC 301.5 and a murine myeloma .
1.4189 10.9365 0.9997 In order to define the roles of these two factors , which bind to the same kappa B enhancers , in transcription activation we have prepared somatic cell hybrids between IARC 301.5 and a cell_linemurine myeloma .
4.3361 20.6421 10.7641 In order to define the roles of these two factors , which bind to the same kappa B enhancers , in transcription activation we have prepared cell_linesomatic cell hybrids between IARC 301.5 and a murine myeloma .
In order to define the roles of these two proteinfactors , which bind to the same kappa B enhancers , in transcription activation we have prepared somatic cell hybrids between IARC 301.5 and a murine myeloma .
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1.5792 10.7516 1.0000 Most hybrids express both KBF1 and proteinNF-kappa B in their nuclei , but one hybrid expresses only KBF1 .
1.5412 10.9372 1.0000 Most hybrids express both proteinKBF1 and NF-kappa B in their nuclei , but one hybrid expresses only KBF1 .
1.5262 10.4149 1.0000 Most hybrids express both KBF1 and NF-kappa B in their nuclei , but one hybrid expresses only proteinKBF1 .
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5.3663 30.7892 20.0404 The kappa B enhancer of the gene encoding the proteininterleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B .
2.2151 20.3732 10.1657 The kappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing nuclear proteinNF-kappa B .
1.6433 20.2076 10.9503 The kappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing proteinnuclear NF-kappa B .
1.2714 20.8065 0.9973 The kappa B enhancer of the gene encoding the proteininterleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B .
0.9490 1.0000 0.9985 The kappa B enhancer of the gene encoding the interleukin-2 ( proteinIL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B .
0.8293 0.9991 0.9999 The kappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( proteinIL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B .
0.6237 0.8573 0.9981 The DNAkappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B .
The kappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R alpha ) is functional only in the cell_linehybrids expressing nuclear NF-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5425 20.7521 10.5903 These findings show that proteinnuclear NF-kappa B is necessary to activate the kappa B enhancer , while KBF1 by itself is not sufficient.
3.4647 20.8856 10.4393 These findings show that nuclear NF-kappa B is necessary to activate the DNAkappa B enhancer , while KBF1 by itself is not sufficient.
2.3849 20.8598 0.9996 These findings show that nuclear NF-kappa B is necessary to activate the kappa B enhancer , while proteinKBF1 by itself is not sufficient.
0.7161 0.9999 0.9999 These findings show that nuclear proteinNF-kappa B is necessary to activate the kappa B enhancer , while KBF1 by itself is not sufficient.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4365 20.1210 1.0000 We propose that KBF1 is a competitive inhibitor of proteinNF-kappa B and discuss how these factors may be involved in the transient expression of IL-2 and IL-2 alpha genes during the immune response .
1.7433 10.2468 1.0000 We propose that proteinKBF1 is a competitive inhibitor of NF-kappa B and discuss how these factors may be involved in the transient expression of IL-2 and IL-2 alpha genes during the immune response .
0.7006 0.9999 0.9998 We propose that KBF1 is a competitive inhibitor of NF-kappa B and discuss how these factors may be involved in the transient expression of proteinIL-2 and IL-2 alpha genes during the immune response .
0.6308 1.0000 0.9983 We propose that KBF1 is a competitive inhibitor of NF-kappa B and discuss how these factors may be involved in the transient expression of IL-2 and proteinIL-2 alpha genes during the immune response .
We propose that KBF1 is a competitive inhibitor of NF-kappa B and discuss how these factors may be involved in the transient expression of IL-2 and proteinIL-2 alpha genes during the immune response .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7545 20.5265 10.4528 T-helper-cell determinants in protein antigens are preferentially located in proteincysteine-rich antigen segments resistant to proteolytic cleavage by cathepsin B , L , and D .
1.5343 10.9344 1.0000 T-helper-cell determinants in proteinprotein antigens are preferentially located in cysteine-rich antigen segments resistant to proteolytic cleavage by cathepsin B , L , and D .
0.8437 0.9976 0.9999 proteinT-helper-cell determinants in protein antigens are preferentially located in cysteine-rich antigen segments resistant to proteolytic cleavage by cathepsin B , L , and D .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1220 20.5020 1.0000 We report on a computer algorithm capable of predicting the location of proteinT-helper-cell epitopes in protein antigen ( Ag ) by analysing the Ag amino acid sequence .
1.4816 10.5702 1.0000 We report on a computer algorithm capable of predicting the location of T-helper-cell epitopes in proteinprotein antigen ( Ag ) by analysing the Ag amino acid sequence .
0.9515 1.0000 1.0000 We report on a computer algorithm capable of predicting the location of T-helper-cell epitopes in protein antigen ( proteinAg ) by analysing the Ag amino acid sequence .
4.7213 20.9204 10.6753 We report on a computer algorithm capable of predicting the location of T-helper-cell epitopes in protein antigen ( Ag ) by analysing the proteinAg amino acid sequence .
We report on a computer algorithm capable of predicting the location of T-helper-cell epitopes in protein antigen ( Ag ) by analysing the proteinAg amino acid sequence .
We report on a computer algorithm capable of predicting the location of T-helper-cell epitopes in protein antigen ( Ag ) by analysing the Ag proteinamino acid sequence .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7992 10.5069 1.0000 The algorithm was constructed with the aim of identifying segments in proteinAg which are resistant to proteolytic degradation by the enzymes cathepsin B , L , and D .
0.8080 1.0000 1.0000 The algorithm was constructed with the aim of identifying segments in Ag which are resistant to proteolytic degradation by the enzymes cathepsin B , proteinL , and D .
0.7677 0.9997 1.0000 The algorithm was constructed with the aim of identifying segments in Ag which are resistant to proteolytic degradation by the enzymes proteincathepsin B , L , and D .
0.5358 1.0000 1.0000 The algorithm was constructed with the aim of identifying segments in Ag which are resistant to proteolytic degradation by the enzymes cathepsin B , L , and proteinD .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6144 20.9491 10.9457 These are prominent enzymes in the endocytic pathway through which proteinsoluble protein Ag enter APC , and resistant segments in Ag may, therefore, be expected to contain more T-cell determinants than susceptible segments .
2.2377 20.4366 1.0000 These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter APC , and resistant segments in Ag may, therefore, be expected to contain more proteinT-cell determinants than susceptible segments .
1.7265 10.7647 1.0000 These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter APC , and resistant segments in proteinAg may, therefore, be expected to contain more T-cell determinants than susceptible segments .
1.5026 10.8748 0.9998 These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter APC , and resistant segments in Ag may, therefore, be expected to contain more T-cell determinants than proteinsusceptible segments .
1.1514 10.7908 0.9999 These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter APC , and proteinresistant segments in Ag may, therefore, be expected to contain more T-cell determinants than susceptible segments .
0.5894 1.0000 1.0000 These are prominent proteinenzymes in the endocytic pathway through which soluble protein Ag enter APC , and resistant segments in Ag may, therefore, be expected to contain more T-cell determinants than susceptible segments .
0.5252 1.0000 1.0000 These are prominent enzymes in the endocytic pathway through which soluble protein proteinAg enter APC , and resistant segments in Ag may, therefore, be expected to contain more T-cell determinants than susceptible segments .
0.8789 0.9999 1.0000 These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter cell_typeAPC , and resistant segments in Ag may, therefore, be expected to contain more T-cell determinants than susceptible segments .
These are prominent enzymes in the endocytic pathway through which soluble protein Ag enter proteinAPC , and resistant segments in Ag may, therefore, be expected to contain more T-cell determinants than susceptible segments .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6901 10.8332 0.9999 From information available in the literature on the substrate specificity of the three enzymes , it is clear that a cysteine is not accepted in any of the S2 , S1 , S1' , and S2' subsites of cathepsin B and L , and not in the S1 and S1' subsites of proteincathepsin D .
0.9394 1.0000 1.0000 From information available in the literature on the substrate specificity of the three proteinenzymes , it is clear that a cysteine is not accepted in any of the S2 , S1 , S1' , and S2' subsites of cathepsin B and L , and not in the S1 and S1' subsites of cathepsin D .
0.7582 1.0000 1.0000 From information available in the literature on the substrate specificity of the three enzymes , it is clear that a cysteine is not accepted in any of the S2 , S1 , S1' , and S2' subsites of cathepsin B and L , and not in the proteinS1 and S1' subsites of cathepsin D .
1.6677 10.0937 0.9999 From information available in the literature on the substrate specificity of the three enzymes , it is clear that a cysteine is not accepted in any of the S2 , S1 , S1' , and S2' subsites of proteincathepsin B and L , and not in the S1 and S1' subsites of cathepsin D .
From information available in the literature on the substrate specificity of the three enzymes , it is clear that a cysteine is not accepted in any of the S2 , S1 , S1' , and S2' subsites of cathepsin B and L , and not in the S1 and proteinS1' subsites of cathepsin D .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8580 30.2826 10.3868 Moreover, we have noticed that proteincysteine -containing T-cell determinants in a number of protein Ag are particularly rich in the amino acids alanine , glycine , lysine , leucine , serine , threonine , and valine .
2.2800 20.8083 1.0000 Moreover, we have noticed that cysteine -containing T-cell determinants in a number of proteinprotein Ag are particularly rich in the amino acids alanine , glycine , lysine , leucine , serine , threonine , and valine .
Moreover, we have noticed that cysteine -containing T-cell determinants in a number of protein proteinAg are particularly rich in the amino acids alanine , glycine , lysine , leucine , serine , threonine , and valine .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5348 20.5375 1.0000 By searching protein Ag for clusters of amino acids containing cysteine and two of the other amino acids we were able to predict 17 out of 23 empirically known proteinT-cell determinants in the Ag with a relatively low number of false (positive) predictions.
0.9489 1.0000 1.0000 By searching protein Ag for clusters of amino acids containing cysteine and two of the other amino acids we were able to predict 17 out of 23 empirically known T-cell determinants in the proteinAg with a relatively low number of false (positive) predictions.
2.5525 20.6343 1.0000 By searching proteinprotein Ag for clusters of amino acids containing cysteine and two of the other amino acids we were able to predict 17 out of 23 empirically known T-cell determinants in the Ag with a relatively low number of false (positive) predictions.
By searching protein proteinAg for clusters of amino acids containing cysteine and two of the other amino acids we were able to predict 17 out of 23 empirically known T-cell determinants in the Ag with a relatively low number of false (positive) predictions.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6360 20.1292 10.6717 Furthermore, we present a new principle for searching Ag for potential proteinamphipatic alpha-helical protein segments .
1.6485 10.1346 1.0000 Furthermore, we present a new principle for searching proteinAg for potential amphipatic alpha-helical protein segments .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5343 20.1555 1.0000 Such segments accord well with empirically known proteinT-cell determinants and our algorithm produces a lower number of false positive predictions than the principle based on discrete Fourier transformations previously described.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1252 10.6109 10.6136 Contribution of NF-kappa B and DNASp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1 : distinct patterns of viral growth are determined by T-cell types .
2.3728 20.5677 0.9998 Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1 : distinct patterns of viral growth are determined by cell_typeT-cell types .
1.5325 10.9298 0.9999 Contribution of proteinNF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1 : distinct patterns of viral growth are determined by T-cell types .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.8605 30.0926 10.8935 Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1 , lacking all the NF-kappa B and Sp1 binding sites present in the DNAnative long terminal repeat ( LTR ), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation .
2.2870 20.5965 1.0000 Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1 , lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat ( LTR ), proviruses containing DNAreconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation .
0.9655 1.0000 1.0000 Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1 , lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat ( DNALTR ), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation .
0.9055 1.0000 1.0000 Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1 , lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat ( LTR ), proviruses containing reconstructed DNALTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9491 20.3796 10.8656 Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different cell_typehuman T-cell types depending on which element (s) was present in the LTR .
1.7820 10.2816 1.0000 Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element (s) was present in the DNALTR .
Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which DNAelement (s) was present in the LTR .
Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human cell_typeT-cell types depending on which element (s) was present in the LTR .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3830 20.7349 10.7224 For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( cell_typeperipheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
2.9535 20.6571 10.8608 For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no DNASp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
1.9880 20.7182 0.7669 For example, in experiments involving proviral clones with LTRs containing one or two proteinNF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
1.8268 10.1302 1.0000 For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than cell_lineH9 greater than CEM greater than Jurkat ) was observed.
1.8226 10.1418 1.0000 For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than cell_lineCEM greater than Jurkat ) was observed.
1.8163 10.2499 1.0000 For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than cell_lineJurkat ) was observed.
1.7400 10.3557 1.0000 For example, in experiments involving proviral clones with DNALTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
1.4149 20.6845 0.9999 For example, in experiments involving proviral clones with LTRs containing one or two DNANF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
0.9343 1.0000 1.0000 For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood lymphocytes = cell_lineMT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites ), a hierarchy of cellular permissivity to virus replication ( peripheral blood cell_typelymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat ) was observed.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9990 20.0141 0.9999 Of note was the associated emergence of second-site LTR revertants which involved an alteration of the DNATATA box .
3.7199 20.4942 10.8002 Of note was the associated emergence of DNAsecond-site LTR revertants which involved an alteration of the TATA box .
Of note was the associated emergence of DNAsecond-site LTR revertants which involved an alteration of the TATA box .
Cls_Score Left_Reg_Score Right_Reg_Score Text
8.8649 40.1497 20.5856 These results suggest that the DNAhuman immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present.
2.1114 20.6606 0.9999 These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different cell_typeT-cell types and is capable of changing depending on the particular combination of transcriptional factors present.
1.9425 20.7005 0.9999 These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of proteintranscriptional factors present.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5646 20.0541 10.7156 Stimulation of DNAinterferon beta gene transcription in vitro by purified NF-kappa B and a novel TH protein .
1.4846 10.7520 1.0000 Stimulation of interferon beta gene transcription in vitro by purified proteinNF-kappa B and a novel TH protein .
1.4278 10.7181 0.9999 Stimulation of interferon beta gene transcription in vitro by purified NF-kappa B and a novel proteinTH protein .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7694 20.4815 0.9999 The human interferon beta ( IFN-beta ) regulatory element consists of multiple DNAenhanson domains which are targets for transcription factors involved in inducible expression of the promoter .
1.7590 20.3725 0.9999 The human interferon beta ( IFN-beta ) regulatory element consists of multiple enhanson domains which are targets for proteintranscription factors involved in inducible expression of the promoter .
1.6677 10.2974 0.9320 The DNAhuman interferon beta ( IFN-beta ) regulatory element consists of multiple enhanson domains which are targets for transcription factors involved in inducible expression of the promoter .
1.3655 10.6247 0.9999 The human interferon beta ( IFN-beta ) regulatory element consists of multiple enhanson domains which are targets for transcription factors involved in inducible expression of the DNApromoter .
0.9372 1.0000 0.9949 The human interferon beta ( proteinIFN-beta ) regulatory element consists of multiple enhanson domains which are targets for transcription factors involved in inducible expression of the promoter .
The proteinhuman interferon beta ( IFN-beta ) regulatory element consists of multiple enhanson domains which are targets for transcription factors involved in inducible expression of the promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.3177 30.5651 10.8871 To further characterize the protein-DNA interactions mediating IFN-beta induction , proteinpositive regulatory domain (PRD) II binding proteins were purified from phorbol ester induced Jurkat T-cells and from IFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
0.7403 0.9997 1.0000 To further characterize the protein-DNA interactions mediating proteinIFN-beta induction , positive regulatory domain (PRD) II binding proteins were purified from phorbol ester induced Jurkat T-cells and from IFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
0.6623 0.9904 0.9996 To further characterize the protein-DNA interactions mediating IFN-beta induction , positive regulatory domain (PRD) II binding proteins were purified from phorbol ester induced cell_lineJurkat T-cells and from IFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
0.6429 1.0000 0.9998 To further characterize the protein-DNA interactions mediating IFN-beta induction , positive regulatory domain (PRD) II binding proteins were purified from phorbol ester induced Jurkat T-cells and from proteinIFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
4.2181 20.6912 10.9140 To further characterize the protein-DNA interactions mediating IFN-beta induction , positive regulatory domain (PRD) II binding proteins were purified from cell_linephorbol ester induced Jurkat T-cells and from IFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
To further characterize the protein-DNA interactions mediating IFN-beta induction , DNApositive regulatory domain (PRD) II binding proteins were purified from phorbol ester induced Jurkat T-cells and from IFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
To further characterize the protein-DNA interactions mediating IFN-beta induction , positive regulatory domain (PRD) II binding proteins were purified from phorbol ester induced Jurkat T-cells and from cell_lineIFN primed, cycloheximide/polyinosinic-polycytidylic acid treated HeLa S3 cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7252 10.2908 1.0000 From cell_lineHeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a major protein of 52 kD and three minor proteins of 82 , 67 , and 43-47 kD --were purified.
1.6700 10.1827 1.0000 From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a major protein of protein52 kD and three minor proteins of 82 , 67 , and 43-47 kD --were purified.
1.6672 10.2824 1.0000 From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from cell_typeT-cells , four proteins--a major protein of 52 kD and three minor proteins of 82 , 67 , and 43-47 kD --were purified.
1.6595 10.1605 0.9999 From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a proteinmajor protein of 52 kD and three minor proteins of 82 , 67 , and 43-47 kD --were purified.
From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a major protein of 52 kD and three proteinminor proteins of 82 , 67 , and 43-47 kD --were purified.
From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a major protein of 52 kD and three minor proteins of protein82 , 67 , and 43-47 kD --were purified.
From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a major protein of 52 kD and three minor proteins of 82 , 67 , and protein43-47 kD --were purified.
From HeLa cells , two major proteins of 52 and 45 kilodaltons (kD) copurified with DNA binding activity , whereas from T-cells , four proteins--a major protein of 52 kD and three minor proteins of 82 , protein67 , and 43-47 kD --were purified.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4660 10.9535 0.9999 Also, an induction specific DNA binding protein was purified from cell_lineHeLa cells that interacted with the ( AAGTGA )4 tetrahexamer sequence and the PRDI domain .
5.8393 30.0025 20.2303 Also, an induction specific DNA binding protein was purified from HeLa cells that interacted with the protein( AAGTGA )4 tetrahexamer sequence and the PRDI domain .
3.4954 20.8589 10.8218 Also, an induction specific proteinDNA binding protein was purified from HeLa cells that interacted with the ( AAGTGA )4 tetrahexamer sequence and the PRDI domain .
1.8409 20.3283 0.9998 Also, an induction specific DNA binding protein was purified from HeLa cells that interacted with the ( AAGTGA )4 tetrahexamer sequence and the proteinPRDI domain .
1.1304 0.9998 10.6269 Also, an induction specific DNA binding protein was purified from HeLa cells that interacted with the ( proteinAAGTGA )4 tetrahexamer sequence and the PRDI domain .
Also, an induction proteinspecific DNA binding protein was purified from HeLa cells that interacted with the ( AAGTGA )4 tetrahexamer sequence and the PRDI domain .
Also, an induction specific DNA binding protein was purified from HeLa cells that interacted with the ( AAGTGA )4 tetrahexamer sequence and the DNAPRDI domain .
Also, an induction specific DNA binding protein was purified from HeLa cells that interacted with the ( AAGTGA )4 DNAtetrahexamer sequence and the PRDI domain .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5383 10.4945 1.0000 This protein is immunologically distinct from proteinIRF-1/ISGF2 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2259 20.9733 10.0065 Uninduced or Sendai virus induced HeLa extracts were used to examine transcription in vitro using a series of DNAIFN beta promoter deletions .
2.6203 20.7207 10.2729 Uninduced or Sendai virus induced HeLa extracts were used to examine transcription in vitro using a series of DNAIFN beta promoter deletions .
0.7119 0.9998 0.9974 Uninduced or Sendai virus induced cell_lineHeLa extracts were used to examine transcription in vitro using a series of IFN beta promoter deletions .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3620 20.5727 1.0000 Deletions upstream of the DNAPRDII element increased transcription in the uninduced extract, indicating predominantly negative regulation of the promoter .
1.7494 10.7519 1.0000 Deletions upstream of the PRDII element increased transcription in the uninduced extract, indicating predominantly negative regulation of the DNApromoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6382 10.9998 1.0000 A 2-4-fold increase in DNAIFN-beta promoter transcription was observed in Sendai virus induced extracts , and deletion of PRDI and PRDII elements decreased this induced level of transcription .
0.7193 0.9999 1.0000 A 2-4-fold increase in IFN-beta promoter transcription was observed in Sendai virus induced extracts , and deletion of DNAPRDI and PRDII elements decreased this induced level of transcription .
0.6563 0.9999 0.9935 A 2-4-fold increase in IFN-beta promoter transcription was observed in Sendai virus induced extracts , and deletion of PRDI and DNAPRDII elements decreased this induced level of transcription .
0.5930 0.9919 0.9999 A 2-4-fold increase in IFN-beta promoter transcription was observed in Sendai virus induced extracts , and deletion of PRDI and DNAPRDII elements decreased this induced level of transcription .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8555 20.9296 10.4024 When purified PRDII and proteintetrahexamer binding proteins were added to the induced extract, a 4-fold increase in transcription was observed.
1.5477 10.3834 10.0044 When proteinpurified PRDII and tetrahexamer binding proteins were added to the induced extract, a 4-fold increase in transcription was observed.
0.8941 0.9999 1.0000 When purified proteinPRDII and tetrahexamer binding proteins were added to the induced extract, a 4-fold increase in transcription was observed.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7751 10.2488 1.0000 These experiments demonstrate that it is possible to modulate IFN-beta transcription in vitro but indicate that additional proteins may be required to fully activate proteinIFN-beta transcription .
1.8081 10.0104 1.0000 These experiments demonstrate that it is possible to modulate proteinIFN-beta transcription in vitro but indicate that additional proteins may be required to fully activate IFN-beta transcription .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8549 20.5001 10.6632 The rhombotin family of DNAcysteine -rich LIM-domain oncogenes : distinct members are involved in T-cell translocations to human chromosomes 11p15 and 11p13 .
1.1761 10.8872 0.9998 The proteinrhombotin family of cysteine -rich LIM-domain oncogenes : distinct members are involved in T-cell translocations to human chromosomes 11p15 and 11p13 .
0.9449 1.0000 1.0000 The rhombotin family of cysteine -rich LIM-domain oncogenes : distinct members are involved in T-cell translocations to human chromosomes 11p15 and DNA11p13 .
0.7672 1.0000 1.0000 The rhombotin family of cysteine -rich LIM-domain oncogenes : distinct members are involved in T-cell translocations to human chromosomes DNA11p15 and 11p13 .
The rhombotin family of cysteine -rich LIM-domain oncogenes : distinct members are involved in DNAT-cell translocations to human chromosomes 11p15 and 11p13 .
The DNArhombotin family of cysteine -rich LIM-domain oncogenes : distinct members are involved in T-cell translocations to human chromosomes 11p15 and 11p13 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0824 10.9433 10.9103 A chromosomal translocation in a T-cell leukemia involving the short arm of DNAhuman chromosome 11 at band 11p15 disrupts the rhombotin gene .
1.6204 10.2285 0.9999 A chromosomal translocation in a T-cell leukemia involving the short arm of human chromosome 11 at DNAband 11p15 disrupts the rhombotin gene .
1.4185 10.9224 0.9998 A chromosomal translocation in a T-cell leukemia involving the short arm of human chromosome 11 at band 11p15 disrupts the DNArhombotin gene .
1.3032 10.5075 0.9999 A chromosomal translocation in a T-cell leukemia involving the DNAshort arm of human chromosome 11 at band 11p15 disrupts the rhombotin gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9052 10.7388 10.6852 This gene encodes a protein with duplicated proteincysteine -rich regions called LIM domains , which show homology to zinc-binding proteins and to iron-sulfur centers of ferredoxins .
1.4960 10.9019 1.0000 This gene encodes a protein with duplicated cysteine -rich regions called LIM domains , which show homology to proteinzinc-binding proteins and to iron-sulfur centers of ferredoxins .
1.4430 10.7796 1.0000 This gene encodes a protein with duplicated cysteine -rich regions called LIM domains , which show homology to zinc-binding proteins and to proteiniron-sulfur centers of ferredoxins .
0.8571 1.0000 1.0000 This gene encodes a protein with duplicated cysteine -rich regions called LIM domains , which show homology to zinc-binding proteins and to iron-sulfur centers of proteinferredoxins .
0.8181 0.9989 1.0000 This gene encodes a protein with duplicated cysteine -rich regions called proteinLIM domains , which show homology to zinc-binding proteins and to iron-sulfur centers of ferredoxins .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2479 20.1454 1.0000 Two homologues of the DNArhombotin gene have now been isolated.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6558 20.5603 10.7778 One of these, designated Rhom-2 , is located on DNAhuman chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all translocation breakpoints at 11p13 are upstream of the Rhom-2 gene .
2.3013 20.7172 0.9999 One of these, designated Rhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all translocation breakpoints at 11p13 are upstream of the DNARhom-2 gene .
1.7868 10.2761 1.0000 One of these, designated Rhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all translocation breakpoints at DNA11p13 are upstream of the Rhom-2 gene .
1.6152 10.3789 1.0000 One of these, designated Rhom-2 , is located on human chromosome 11 at DNAband 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all translocation breakpoints at 11p13 are upstream of the Rhom-2 gene .
0.8860 1.0000 1.0000 One of these, designated DNARhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all translocation breakpoints at 11p13 are upstream of the Rhom-2 gene .
1.0408 10.5719 0.9999 One of these, designated Rhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all DNAtranslocation breakpoints at 11p13 are upstream of the Rhom-2 gene .
One of these, designated Rhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of T-cell leukemia-specific translocations occur; all translocation breakpoints at 11p13 are upstream of the DNARhom-2 gene .
One of these, designated Rhom-2 , is located on human chromosome 11 at band 11p13 , where a cluster of DNAT-cell leukemia-specific translocations occur; all translocation breakpoints at 11p13 are upstream of the Rhom-2 gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1547 20.9397 20.4349 Human and mouse Rhom-2 are highly conserved and, like rhombotin , encode two proteintandem cysteine -rich LIM domains .
1.4530 10.2204 1.0000 Human and mouse Rhom-2 are highly conserved and, like proteinrhombotin , encode two tandem cysteine -rich LIM domains .
0.8257 1.0000 1.0000 Human and mouse proteinRhom-2 are highly conserved and, like rhombotin , encode two tandem cysteine -rich LIM domains .
Human and mouse Rhom-2 are highly conserved and, like rhombotin , encode two tandem cysteine -rich proteinLIM domains .
Human and mouse Rhom-2 are highly conserved and, like rhombotin , encode two DNAtandem cysteine -rich LIM domains .
Human and mouse Rhom-2 are highly conserved and, like DNArhombotin , encode two tandem cysteine -rich LIM domains .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9401 0.9986 1.0000 RNARhom-2 mRNA is expressed in early mouse development in central nervous system , lung , kidney , liver , and spleen but only very low levels occur in thymus .
0.9272 1.0000 0.9915 proteinRhom-2 mRNA is expressed in early mouse development in central nervous system , lung , kidney , liver , and spleen but only very low levels occur in thymus .
DNARhom-2 mRNA is expressed in early mouse development in central nervous system , lung , kidney , liver , and spleen but only very low levels occur in thymus .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1159 20.9836 0.9999 The other gene, designated Rhom-3 , is not on chromosome 11 but also retains homology to the DNALIM domain of rhombotin .
1.7163 10.8771 1.0000 The other gene, designated DNARhom-3 , is not on chromosome 11 but also retains homology to the LIM domain of rhombotin .
2.2959 20.6039 1.0000 The other gene, designated Rhom-3 , is not on DNAchromosome 11 but also retains homology to the LIM domain of rhombotin .
1.5959 10.2034 1.0000 The other gene, designated Rhom-3 , is not on chromosome 11 but also retains homology to the LIM domain of proteinrhombotin .
The other gene, designated Rhom-3 , is not on chromosome 11 but also retains homology to the LIM domain of DNArhombotin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3893 20.2098 1.0000 Since the DNARhom-2 gene is such a common site of chromosomal damage in T-cell tumors , the consistency of translocations near the rhombotin gene was further examined.
2.3350 20.6580 1.0000 Since the Rhom-2 gene is such a common site of chromosomal damage in T-cell tumors , the consistency of translocations near the DNArhombotin gene was further examined.
2.0999 20.7340 0.9881 Since the Rhom-2 gene is such a common site of chromosomal damage in T-cell tumors , the consistency of translocations near the proteinrhombotin gene was further examined.
Since the DNARhom-2 gene is such a common site of chromosomal damage in T-cell tumors , the consistency of translocations near the rhombotin gene was further examined.
Since the Rhom-2 gene is such a common site of chromosomal damage in T-cell tumors , the consistency of translocations near the DNArhombotin gene was further examined.
Since the Rhom-2 gene is such a common site of chromosomal damage in cell_typeT-cell tumors , the consistency of translocations near the rhombotin gene was further examined.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6949 10.5797 1.0000 A second translocation adjacent to proteinrhombotin was found and at the same position as in the previous example.
A second translocation adjacent to DNArhombotin was found and at the same position as in the previous example.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8390 10.2425 1.0000 Therefore, chromosome bands 11p15 ( rhombotin ) and DNA11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved.
1.6566 20.5864 1.0000 Therefore, chromosome bands 11p15 ( rhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the DNA11p15 target more rarely involved.
0.9340 1.0000 1.0000 Therefore, chromosome bands 11p15 ( rhombotin ) and 11p13 ( DNARhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved.
0.9231 1.0000 1.0000 Therefore, chromosome bands 11p15 ( DNArhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved.
2.1800 20.6310 0.9941 Therefore, chromosome bands 11p15 ( rhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the DNA11p15 target more rarely involved.
1.4393 10.7966 0.9977 Therefore, DNAchromosome bands 11p15 ( rhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved.
0.9520 0.9999 1.0000 Therefore, chromosome bands DNA11p15 ( rhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved.
Therefore, DNAchromosome bands 11p15 ( rhombotin ) and 11p13 ( Rhom-2 ) are consistent sites of chromosome translocation in T-cell leukemia , with the 11p15 target more rarely involved.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8078 10.7910 10.4494 The results define the rhombotin gene family as a class of T-cell oncogenes with duplicated DNAcysteine -rich LIM domains .
1.2878 10.9000 0.9999 The results define the rhombotin gene family as a class of DNAT-cell oncogenes with duplicated cysteine -rich LIM domains .
2.8682 20.2298 10.8491 The results define the DNArhombotin gene family as a class of T-cell oncogenes with duplicated cysteine -rich LIM domains .
1.1961 10.5411 0.9931 The results define the proteinrhombotin gene family as a class of T-cell oncogenes with duplicated cysteine -rich LIM domains .
The results define the rhombotin gene family as a class of T-cell oncogenes with duplicated cysteine -rich proteinLIM domains .
The results define the DNArhombotin gene family as a class of T-cell oncogenes with duplicated cysteine -rich LIM domains .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1044 30.8309 10.9894 NF-kappa B activation by tumor necrosis factor alpha in the cell_lineJurkat T cell line is independent of protein kinase A , protein kinase C , and Ca(2+) -regulated kinases .
4.1250 20.7384 10.8227 NF-kappa B activation by proteintumor necrosis factor alpha in the Jurkat T cell line is independent of protein kinase A , protein kinase C , and Ca(2+) -regulated kinases .
3.7844 20.8491 10.9362 NF-kappa B activation by tumor necrosis factor alpha in the Jurkat T cell line is independent of proteinprotein kinase A , protein kinase C , and Ca(2+) -regulated kinases .
3.1867 20.7065 10.5494 NF-kappa B activation by tumor necrosis factor alpha in the Jurkat T cell line is independent of protein kinase A , protein kinase C , and proteinCa(2+) -regulated kinases .
2.8511 10.4917 10.2114 NF-kappa B activation by tumor necrosis factor alpha in the Jurkat T cell line is independent of protein kinase A , proteinprotein kinase C , and Ca(2+) -regulated kinases .
0.8688 0.9999 1.0000 proteinNF-kappa B activation by tumor necrosis factor alpha in the Jurkat T cell line is independent of protein kinase A , protein kinase C , and Ca(2+) -regulated kinases .
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3.2643 30.4345 10.8613 NF-kappa B is a proteinDNA-binding regulatory factor able to control transcription of a number of genes, including human immunodeficiency virus ( HIV ) genes .
3.1680 30.7083 10.8504 NF-kappa B is a DNA-binding regulatory factor able to control transcription of a number of genes, including DNAhuman immunodeficiency virus ( HIV ) genes .
0.8864 0.9998 1.0000 proteinNF-kappa B is a DNA-binding regulatory factor able to control transcription of a number of genes, including human immunodeficiency virus ( HIV ) genes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2428 20.6271 10.4982 In T cells , NF-kappa B is activated upon cellular treatment by phorbol esters and the cytokine proteintumor necrosis factor alpha ( TNF alpha ).
2.1930 10.9030 10.1708 In cell_typeT cells , NF-kappa B is activated upon cellular treatment by phorbol esters and the cytokine tumor necrosis factor alpha ( TNF alpha ).
1.7017 10.0101 0.9999 In T cells , NF-kappa B is activated upon cellular treatment by phorbol esters and the cytokine tumor necrosis factor alpha ( proteinTNF alpha ).
1.5068 10.7111 0.9999 In T cells , proteinNF-kappa B is activated upon cellular treatment by phorbol esters and the cytokine tumor necrosis factor alpha ( TNF alpha ).
1.2933 10.4250 0.9996 In T cells , NF-kappa B is activated upon cellular treatment by phorbol esters and the proteincytokine tumor necrosis factor alpha ( TNF alpha ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8456 20.9621 10.9019 In the present work, we investigated the molecular events leading to NF-kappa B activation by TNF alpha in a cell_linehuman T cell line ( Jurkat ) and its subclone JCT6 , which presents a deficiency in the PKA transduction pathway .
2.2656 20.0359 1.0000 In the present work, we investigated the molecular events leading to proteinNF-kappa B activation by TNF alpha in a human T cell line ( Jurkat ) and its subclone JCT6 , which presents a deficiency in the PKA transduction pathway .
1.6678 10.5330 1.0000 In the present work, we investigated the molecular events leading to NF-kappa B activation by TNF alpha in a human T cell line ( Jurkat ) and its subclone JCT6 , which presents a deficiency in the proteinPKA transduction pathway .
1.4832 10.8109 1.0000 In the present work, we investigated the molecular events leading to NF-kappa B activation by proteinTNF alpha in a human T cell line ( Jurkat ) and its subclone JCT6 , which presents a deficiency in the PKA transduction pathway .
0.9735 1.0000 1.0000 In the present work, we investigated the molecular events leading to NF-kappa B activation by TNF alpha in a human T cell line ( Jurkat ) and its subclone cell_lineJCT6 , which presents a deficiency in the PKA transduction pathway .
0.9417 1.0000 1.0000 In the present work, we investigated the molecular events leading to NF-kappa B activation by TNF alpha in a human T cell line ( cell_lineJurkat ) and its subclone JCT6 , which presents a deficiency in the PKA transduction pathway .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2298 20.1348 0.9999 We found that in both cell lines, both phorbol ester and TNF alpha were able to activate proteinNF-kappa B .
2.2253 20.2848 1.0000 We found that in both cell lines, both phorbol ester and proteinTNF alpha were able to activate NF-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6037 10.8550 1.0000 Phorbol activation was positively modulated by Ca2+ influx while proteinTNF alpha activation was not.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6786 10.4544 1.0000 Furthermore, while PMA activation was inhibited by the proteinPKC inhibitor staurosporin , the TNF alpha effect was unchanged.
1.6129 10.7692 1.0000 Furthermore, while PMA activation was inhibited by the PKC inhibitor staurosporin , the proteinTNF alpha effect was unchanged.
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9577 1.0000 1.0000 proteinTNF alpha did not activate cAMP production and its signal was not modulated by cAMP activators .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5559 10.4563 0.9997 Moreover, cAMP activators did not activate NF-kappa B in cell_lineJurkat cells .
1.4921 10.6488 1.0000 Moreover, cAMP activators did not activate proteinNF-kappa B in Jurkat cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1292 20.3734 10.7791 Thus, TNF alpha -induced NF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as proteinprotein kinase C ( PKC ), protein kinase A , or Ca(2+)-regulated kinases .
2.9100 10.9779 10.6512 Thus, TNF alpha -induced NF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as protein kinase C ( PKC ), proteinprotein kinase A , or Ca(2+)-regulated kinases .
2.0203 20.2389 0.9999 Thus, TNF alpha -induced NF-kappa B activation was found to be mediated by none of the major proteinsignal-mediating kinases such as protein kinase C ( PKC ), protein kinase A , or Ca(2+)-regulated kinases .
1.9947 20.2263 0.9998 Thus, TNF alpha -induced NF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as protein kinase C ( PKC ), protein kinase A , or proteinCa(2+)-regulated kinases .
1.5048 10.6093 1.0000 Thus, TNF alpha -induced proteinNF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as protein kinase C ( PKC ), protein kinase A , or Ca(2+)-regulated kinases .
0.9625 1.0000 1.0000 Thus, TNF alpha -induced NF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as protein kinase C ( proteinPKC ), protein kinase A , or Ca(2+)-regulated kinases .
0.7554 0.9964 1.0000 Thus, proteinTNF alpha -induced NF-kappa B activation was found to be mediated by none of the major signal-mediating kinases such as protein kinase C ( PKC ), protein kinase A , or Ca(2+)-regulated kinases .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2347 20.1627 1.0000 Furthermore, we found that cytoplasmic acidification facilitated proteinNF-kappa B activation by both TNF alpha and PKC , by a mechanism that increases NF-kappa B /I kappa B dissociation without affecting the NF-kappa B translocation step .
2.2241 20.4541 1.0000 Furthermore, we found that cytoplasmic acidification facilitated NF-kappa B activation by both TNF alpha and PKC , by a mechanism that increases NF-kappa B /I kappa B dissociation without affecting the proteinNF-kappa B translocation step .
2.2021 20.1041 0.9992 Furthermore, we found that cytoplasmic acidification facilitated NF-kappa B activation by both TNF alpha and PKC , by a mechanism that increases proteinNF-kappa B /I kappa B dissociation without affecting the NF-kappa B translocation step .
1.4950 10.8736 1.0000 Furthermore, we found that cytoplasmic acidification facilitated NF-kappa B activation by both proteinTNF alpha and PKC , by a mechanism that increases NF-kappa B /I kappa B dissociation without affecting the NF-kappa B translocation step .
1.4574 0.9223 10.5283 Furthermore, we found that cytoplasmic acidification facilitated NF-kappa B activation by both TNF alpha and PKC , by a mechanism that increases NF-kappa B protein/I kappa B dissociation without affecting the NF-kappa B translocation step .
0.9168 1.0000 1.0000 Furthermore, we found that cytoplasmic acidification facilitated NF-kappa B activation by both TNF alpha and proteinPKC , by a mechanism that increases NF-kappa B /I kappa B dissociation without affecting the NF-kappa B translocation step .
1.9162 20.9514 10.1496 Furthermore, we found that cytoplasmic acidification facilitated NF-kappa B activation by both TNF alpha and PKC , by a mechanism that increases proteinNF-kappa B /I kappa B dissociation without affecting the NF-kappa B translocation step .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8654 10.9643 10.7932 The functional domains of the DNAmurine Thy-1 gene promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6830 20.3032 1.0000 The Thy-1 gene promoter resembles a "housekeeping" promoter in that it is located within a methylation-free island , lacks a canonical TATA box , and displays heterogeneity in the 5'-end termini of the RNAmRNA .
2.1255 20.3919 0.9999 The Thy-1 gene promoter resembles a DNA"housekeeping" promoter in that it is located within a methylation-free island , lacks a canonical TATA box , and displays heterogeneity in the 5'-end termini of the mRNA .
1.4556 20.8472 0.9999 The Thy-1 gene promoter resembles a "housekeeping" promoter in that it is located within a DNAmethylation-free island , lacks a canonical TATA box , and displays heterogeneity in the 5'-end termini of the mRNA .
1.4356 10.5595 0.9987 The DNAThy-1 gene promoter resembles a "housekeeping" promoter in that it is located within a methylation-free island , lacks a canonical TATA box , and displays heterogeneity in the 5'-end termini of the mRNA .
2.1439 20.7755 1.0000 The Thy-1 gene promoter resembles a "housekeeping" promoter in that it is located within a methylation-free island , lacks a canonical DNATATA box , and displays heterogeneity in the 5'-end termini of the mRNA .
The Thy-1 gene promoter resembles a "housekeeping" promoter in that it is located within a methylation-free island , lacks a canonical TATA box , and displays heterogeneity in the RNA5'-end termini of the mRNA .
The Thy-1 gene promoter resembles a "housekeeping" promoter in that it is located within a methylation-free island , lacks a DNAcanonical TATA box , and displays heterogeneity in the 5'-end termini of the mRNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Using transgenic mice , we show that this DNApromoter does not confer any tissue specificity and is active only in a position-dependent manner .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4660 20.2564 0.9999 It can only be activated in a tissue-specific manner by elements that lie downstream of the DNAinitiation site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1218 30.0276 10.8431 We have analyzed the functional domains of the DNAminimal Thy-1 promoter and show that the dominant promoter elements consist of multiple binding sites for the transcription factor Sp1 , an inverted CCAAT box , and sequences proximal to the transcription start site .
3.3788 30.6036 10.5975 We have analyzed the functional domains of the minimal Thy-1 promoter and show that the dominant promoter elements consist of DNAmultiple binding sites for the transcription factor Sp1 , an inverted CCAAT box , and sequences proximal to the transcription start site .
2.5829 20.6241 10.7343 We have analyzed the functional domains of the minimal Thy-1 promoter and show that the DNAdominant promoter elements consist of multiple binding sites for the transcription factor Sp1 , an inverted CCAAT box , and sequences proximal to the transcription start site .
2.0855 20.5331 0.9999 We have analyzed the functional domains of the minimal Thy-1 promoter and show that the dominant promoter elements consist of multiple binding sites for the transcription factor Sp1 , an inverted DNACCAAT box , and sequences proximal to the transcription start site .
1.3699 20.6558 0.9992 We have analyzed the functional domains of the minimal Thy-1 promoter and show that the dominant promoter elements consist of multiple binding sites for the transcription factor Sp1 , an inverted CCAAT box , and sequences proximal to the DNAtranscription start site .
1.3455 20.7476 0.9992 We have analyzed the functional domains of the minimal Thy-1 promoter and show that the dominant promoter elements consist of multiple binding sites for the proteintranscription factor Sp1 , an inverted CCAAT box , and sequences proximal to the transcription start site .
0.9644 1.0000 1.0000 We have analyzed the functional domains of the minimal Thy-1 promoter and show that the dominant promoter elements consist of multiple binding sites for the transcription factor proteinSp1 , an inverted CCAAT box , and sequences proximal to the transcription start site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2151 20.5885 1.0000 DNase I and gel mobility shift assays show the binding of a number of proteinnuclear factors to these elements , including Sp1 and CP1 .
1.5457 10.9100 1.0000 DNase I and gel mobility shift assays show the binding of a number of nuclear factors to these elements , including proteinSp1 and CP1 .
0.8640 0.9999 1.0000 DNase I and gel mobility shift assays show the binding of a number of nuclear factors to these elements , including Sp1 and proteinCP1 .
0.9103 0.9999 1.0000 proteinDNase I and gel mobility shift assays show the binding of a number of nuclear factors to these elements , including Sp1 and CP1 .
DNase I and gel mobility shift assays show the binding of a number of nuclear factors to these DNAelements , including Sp1 and CP1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3326 20.3173 0.9996 Our results show that the structure of this promoter only permits productive interactions of the two proteintranscription factors Sp1 and CP1 with the basal transcription machinery in the presence of enhancer sequences .
2.3090 20.3468 0.9999 Our results show that the structure of this promoter only permits productive interactions of the two transcription factors Sp1 and CP1 with the basal transcription machinery in the presence of DNAenhancer sequences .
0.9871 1.0000 1.0000 Our results show that the structure of this promoter only permits productive interactions of the two transcription factors Sp1 and proteinCP1 with the basal transcription machinery in the presence of enhancer sequences .
0.9787 1.0000 1.0000 Our results show that the structure of this promoter only permits productive interactions of the two transcription factors proteinSp1 and CP1 with the basal transcription machinery in the presence of enhancer sequences .
Our results show that the structure of this DNApromoter only permits productive interactions of the two transcription factors Sp1 and CP1 with the basal transcription machinery in the presence of enhancer sequences .
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1.8226 20.2840 0.9996 Nuclear factor kappa B activates proenkephalin transcription in cell_typeT lymphocytes .
1.6358 0.9985 10.9769 proteinNuclear factor kappa B activates proenkephalin transcription in T lymphocytes .
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2.5179 20.0482 1.0000 Upon activation, T lymphocytes accumulate high levels of the neuropeptide enkephalin which correlate with high levels of RNAproenkephalin mRNA in the cells.
1.5760 10.4807 0.9999 Upon activation, cell_typeT lymphocytes accumulate high levels of the neuropeptide enkephalin which correlate with high levels of proenkephalin mRNA in the cells.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4123 30.1602 10.7495 The proenkephalin promoter contains a sequence GGGGACGTCCCC , named B2 , which is similar to the DNAkappa B sequence GGGGACTTTCC , the binding site of the transcription factor nuclear factor (NF)-kappa B .
0.8616 1.0000 1.0000 The proenkephalin promoter contains a sequence GGGGACGTCCCC , named DNAB2 , which is similar to the kappa B sequence GGGGACTTTCC , the binding site of the transcription factor nuclear factor (NF)-kappa B .
4.7942 30.6474 20.6027 The proenkephalin promoter contains a sequence GGGGACGTCCCC , named B2 , which is similar to the kappa B sequence GGGGACTTTCC , the binding site of the proteintranscription factor nuclear factor (NF)-kappa B .
1.2726 10.5987 0.9999 The DNAproenkephalin promoter contains a sequence GGGGACGTCCCC , named B2 , which is similar to the kappa B sequence GGGGACTTTCC , the binding site of the transcription factor nuclear factor (NF)-kappa B .
The proenkephalin promoter contains a sequence GGGGACGTCCCC , named B2 , which is similar to the kappa B sequence GGGGACTTTCC , the binding site of the proteintranscription factor nuclear factor (NF)-kappa B .
The proenkephalin promoter contains a sequence GGGGACGTCCCC , named B2 , which is similar to the kappa B sequence GGGGACTTTCC , the binding site of the transcription factor proteinnuclear factor (NF)-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1687 20.1565 0.9999 Activation of cell_typeT lymphocytes induces an NF-kappa B -like binding activity to the B2 site, concomitant with activation of the proenkephalin promoter .
2.1393 20.2648 0.9999 Activation of T lymphocytes induces an NF-kappa B -like binding activity to the B2 site, concomitant with activation of the DNAproenkephalin promoter .
1.5219 10.8909 1.0000 Activation of T lymphocytes induces an proteinNF-kappa B -like binding activity to the B2 site, concomitant with activation of the proenkephalin promoter .
Activation of T lymphocytes induces an NF-kappa B -like binding activity to the DNAB2 site, concomitant with activation of the proenkephalin promoter .
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2.2468 20.1993 1.0000 Mutations at the DNAB2 site abolish this transcriptional activation .
Mutations at the DNAB2 site abolish this transcriptional activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1793 20.0117 1.0000 The purified homodimer (two p50s ) of the proteinDNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
1.8300 10.1165 1.0000 The purified homodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two proteinp50s ) form of the factor.
1.6160 10.5268 1.0000 The purified homodimer (two p50s ) of the DNA-binding subunit of proteinNF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
0.9134 1.0000 1.0000 The purified homodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two proteinp65s plus two p50s ) form of the factor.
0.9061 1.0000 1.0000 The purified homodimer (two proteinp50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
0.6910 1.0000 1.0000 The purified homodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the proteinheterotetramer (two p65s plus two p50s ) form of the factor.
1.4893 10.6857 0.9999 The purified homodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the DNAB2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
1.0176 10.1669 1.0000 The proteinpurified homodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
The purified proteinhomodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the B2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
The purified homodimer (two p50s ) of the DNA-binding subunit of NF-kappa B binds the DNAB2 site of proenkephalin relatively better than does the heterotetramer (two p65s plus two p50s ) form of the factor.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2405 20.0459 1.0000 Thus, it appears that the T-cell-specific activation of the DNAproenkephalin promoter is mediated by NF-kappa B .
1.4861 10.8746 1.0000 Thus, it appears that the T-cell-specific activation of the proenkephalin promoter is mediated by proteinNF-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2960 20.9077 1.0000 However, as NF-kappa B is ubiquitous and the transcriptional activation through the B2 site is T cell specific , yet another proteinT-cell-specific factor which synergizes with NF-kappa B should be considered.
2.2874 20.4263 1.0000 However, as NF-kappa B is ubiquitous and the transcriptional activation through the B2 site is T cell specific , yet another T-cell-specific factor which synergizes with proteinNF-kappa B should be considered.
1.5790 10.9258 1.0000 However, as proteinNF-kappa B is ubiquitous and the transcriptional activation through the B2 site is T cell specific , yet another T-cell-specific factor which synergizes with NF-kappa B should be considered.
2.1580 20.1886 1.0000 However, as NF-kappa B is ubiquitous and the transcriptional activation through the DNAB2 site is T cell specific , yet another T-cell-specific factor which synergizes with NF-kappa B should be considered.
0.5534 0.9988 0.9994 However, as NF-kappa B is ubiquitous and the transcriptional activation through the B2 site is cell_typeT cell specific , yet another T-cell-specific factor which synergizes with NF-kappa B should be considered.
However, as NF-kappa B is ubiquitous and the transcriptional activation through the DNAB2 site is T cell specific , yet another T-cell-specific factor which synergizes with NF-kappa B should be considered.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5783 10.9004 1.0000 Induction of proteinNF-KB during monocyte differentiation by HIV type 1 infection .
Induction of NF-KB during cell_typemonocyte differentiation by HIV type 1 infection .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5461 20.3188 10.7881 The production of human immunodeficiency virus type 1 ( HIV-1 ) progeny was followed in the cell_lineU937 promonocytic cell line after stimulation either with retinoic acid or PMA , and in purified human monocytes and macrophages .
2.4739 30.2877 30.8365 The production of cell_typehuman immunodeficiency virus type 1 ( HIV-1 ) progeny was followed in the U937 promonocytic cell line after stimulation either with retinoic acid or PMA , and in purified human monocytes and macrophages .
1.9057 30.4736 10.4148 The production of human immunodeficiency virus type 1 ( HIV-1 ) progeny was followed in the U937 promonocytic cell line after stimulation either with retinoic acid or PMA , and in cell_typepurified human monocytes and macrophages .
0.8535 0.9999 0.9999 The production of human immunodeficiency virus type 1 ( HIV-1 ) progeny was followed in the U937 promonocytic cell line after stimulation either with retinoic acid or PMA , and in purified human monocytes and cell_typemacrophages .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5842 20.2976 10.8167 Electrophoretic mobility shift assays and Southwestern blotting experiments were used to detect the binding of cellular transactivation factor NF-KB to the DNAdouble repeat-KB enhancer sequence located in the long terminal repeat .
4.0348 30.2543 10.9453 Electrophoretic mobility shift assays and Southwestern blotting experiments were used to detect the binding of proteincellular transactivation factor NF-KB to the double repeat-KB enhancer sequence located in the long terminal repeat .
3.4208 20.9610 10.4553 Electrophoretic mobility shift assays and Southwestern blotting experiments were used to detect the binding of cellular transactivation factor NF-KB to the double repeat-KB enhancer sequence located in the DNAlong terminal repeat .
0.9822 1.0000 1.0000 Electrophoretic mobility shift assays and Southwestern blotting experiments were used to detect the binding of cellular transactivation factor proteinNF-KB to the double repeat-KB enhancer sequence located in the long terminal repeat .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3990 20.6173 1.0000 PMA treatment , and not retinoic acid treatment of the cell_lineU937 cells acts in inducing NF-KB expression in the nuclei .
1.6796 10.4775 1.0000 PMA treatment , and not retinoic acid treatment of the U937 cells acts in inducing proteinNF-KB expression in the nuclei .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4836 20.0798 1.0000 In nuclear extracts from monocytes or macrophages , induction of proteinNF-KB occurred only if the cells were previously infected with HIV-1 .
1.6276 10.7965 1.0000 In nuclear extracts from cell_typemonocytes or macrophages , induction of NF-KB occurred only if the cells were previously infected with HIV-1 .
0.9074 0.9999 1.0000 In nuclear extracts from monocytes or cell_typemacrophages , induction of NF-KB occurred only if the cells were previously infected with HIV-1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3938 20.5459 0.9963 When U937 cells were infected with HIV-1 , no induction of proteinNF-KB factor was detected, whereas high level of progeny virions was produced, suggesting that this factor was not required for viral replication .
2.3199 20.7368 1.0000 When U937 cells were infected with HIV-1 , no induction of proteinNF-KB factor was detected, whereas high level of progeny virions was produced, suggesting that this factor was not required for viral replication .
1.7641 10.6058 1.0000 When cell_lineU937 cells were infected with HIV-1 , no induction of NF-KB factor was detected, whereas high level of progeny virions was produced, suggesting that this factor was not required for viral replication .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8212 20.5316 10.5212 These results indicate that in cell_linemonocytic cell lineage , HIV-1 could mimic some differentiation/activation stimuli allowing nuclear NF-KB expression .
1.5202 10.9287 1.0000 These results indicate that in monocytic cell lineage , HIV-1 could mimic some differentiation/activation stimuli allowing nuclear proteinNF-KB expression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4153 20.3379 10.5539 Disruption of the DNAhuman SCL locus by " illegitimate" V-(D)-J recombinase activity .
1.4541 10.9675 0.9999 Disruption of the human SCL locus by " illegitimate" proteinV-(D)-J recombinase activity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5708 30.2303 10.8853 A fusion complementary DNA in the cell_lineT cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor SCL .
2.4791 10.9029 10.2769 A DNAfusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor SCL .
0.9643 0.9999 1.0000 A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor proteinSCL .
4.2499 30.7171 10.6819 A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the proteinputative hematopoietic transcription factor SCL .
A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative proteinhematopoietic transcription factor SCL .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6987 20.0240 10.5916 The fusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( DNASCL interrupting locus ), and the 5' untranslated region of SCL .
3.5649 20.5494 10.6207 The fusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( SCL interrupting locus ), and the DNA5' untranslated region of SCL .
1.4745 10.9124 0.9999 The DNAfusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( SCL interrupting locus ), and the 5' untranslated region of SCL .
0.8948 1.0000 1.0000 The fusion cDNA results from an interstitial deletion between a previously unknown locus , DNASIL ( SCL interrupting locus ), and the 5' untranslated region of SCL .
0.8861 1.0000 1.0000 The fusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( SCL interrupting locus ), and the 5' untranslated region of DNASCL .
The fusion cDNA results from an interstitial deletion between a previously DNAunknown locus , SIL ( SCL interrupting locus ), and the 5' untranslated region of SCL .
The fusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( proteinSCL interrupting locus ), and the 5' untranslated region of SCL .
The fusion cDNA results from an interstitial deletion between a previously unknown locus , SIL ( SCL interrupting locus ), and the 5' untranslated region of proteinSCL .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8885 20.4589 10.4588 Similar to 1;14 translocations , this deletion disrupts the DNASCL 5' regulatory region .
Similar to 1;14 translocations , this deletion disrupts the proteinSCL 5' regulatory region .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3112 20.6427 10.6053 This event is probably mediated by V-(D)-J recombinase activity , although neither locus is an immunoglobulin or a proteinT cell receptor .
1.5387 10.7455 1.0000 This event is probably mediated by V-(D)-J recombinase activity , although neither locus is an proteinimmunoglobulin or a T cell receptor .
1.5986 10.9526 1.0000 This event is probably mediated by proteinV-(D)-J recombinase activity , although neither locus is an immunoglobulin or a T cell receptor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5663 20.0219 10.6461 Two other cell_lineT cell lines , CEM and RPMI 8402 , have essentially identical deletions.
0.9217 1.0000 1.0000 Two other T cell lines , cell_lineCEM and RPMI 8402 , have essentially identical deletions.
0.8084 0.9989 0.9999 Two other T cell lines , CEM and cell_lineRPMI 8402 , have essentially identical deletions.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5786 10.9185 1.0000 Thus, in cell_typelymphocytes , growth-affecting genes other than immune receptors risk rearrangements .
1.4681 10.7590 0.9999 Thus, in lymphocytes , DNAgrowth-affecting genes other than immune receptors risk rearrangements .
1.3627 10.7429 1.0000 Thus, in lymphocytes , growth-affecting genes other than proteinimmune receptors risk rearrangements .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7353 20.5074 10.7168 Thyroid hormone receptors form distinct nuclear protein- dependent and independent complexes with a DNAthyroid hormone response element .
1.5242 0.9987 10.8481 proteinThyroid hormone receptors form distinct nuclear protein- dependent and independent complexes with a thyroid hormone response element .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.3290 30.2260 20.3261 We have examined the binding of nuclear proteins and recombinant thyroid hormone receptors ( TRs ) to the DNApalindromic thyroid hormone responsive element AGGTCATGACCT ( TREp ) using a gel electrophoretic mobility shift assay .
1.3935 10.7025 0.9999 We have examined the binding of proteinnuclear proteins and recombinant thyroid hormone receptors ( TRs ) to the palindromic thyroid hormone responsive element AGGTCATGACCT ( TREp ) using a gel electrophoretic mobility shift assay .
0.9742 1.0000 1.0000 We have examined the binding of nuclear proteins and recombinant thyroid hormone receptors ( proteinTRs ) to the palindromic thyroid hormone responsive element AGGTCATGACCT ( TREp ) using a gel electrophoretic mobility shift assay .
0.9530 1.0000 1.0000 We have examined the binding of nuclear proteins and recombinant thyroid hormone receptors ( TRs ) to the palindromic thyroid hormone responsive element AGGTCATGACCT ( DNATREp ) using a gel electrophoretic mobility shift assay .
2.2150 10.7866 10.7863 We have examined the binding of nuclear proteins and recombinant proteinthyroid hormone receptors ( TRs ) to the palindromic thyroid hormone responsive element AGGTCATGACCT ( TREp ) using a gel electrophoretic mobility shift assay .
We have examined the binding of nuclear proteins and proteinrecombinant thyroid hormone receptors ( TRs ) to the palindromic thyroid hormone responsive element AGGTCATGACCT ( TREp ) using a gel electrophoretic mobility shift assay .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5676 20.5793 10.9232 Four specific protein-DNA complexes were detected after incubation of nuclear extracts ( NE ) from cell_lineT3-responsive pituitary (GH3) cells with a TREp -containing DNA fragment .
3.6381 20.2442 10.5725 Four specific protein-DNA complexes were detected after incubation of nuclear extracts ( NE ) from T3-responsive pituitary (GH3) cells with a DNATREp -containing DNA fragment .
2.0096 20.4921 1.0000 Four specific proteinprotein-DNA complexes were detected after incubation of nuclear extracts ( NE ) from T3-responsive pituitary (GH3) cells with a TREp -containing DNA fragment .
1.4981 10.5081 0.9967 Four specific protein-DNA complexes were detected after incubation of nuclear extracts ( NE ) from T3-responsive pituitary (GH3) cells with a DNATREp -containing DNA fragment .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8357 10.8366 10.9834 This was compared with the TREp binding of proteinreticulocyte lysate-synthesized TRs .
1.4490 10.6195 1.0000 This was compared with the DNATREp binding of reticulocyte lysate-synthesized TRs .
This was compared with the TREp binding of reticulocyte lysate-synthesized proteinTRs .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8144 20.0208 10.2641 TR alpha 1 and proteinTR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
3.6101 20.8098 10.9538 TR alpha 1 and TR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while proteinTR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
2.2153 20.6854 1.0000 TR alpha 1 and TR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to DNATREp as an oligomer .
2.0587 20.7345 10.7276 TR alpha 1 and TR beta 2 each formed a single major proteinTR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
1.5581 0.9984 10.3210 proteinTR alpha 1 and TR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
1.4657 10.2170 0.9981 TR alpha 1 and TR beta 2 each formed a single major proteinTR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
0.6228 1.0000 0.9656 TR alpha 1 and TR beta 2 each formed a single major TR : DNATREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
1.4456 10.8302 1.0000 TR alpha 1 and TR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by proteinGH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
0.5667 0.9858 0.9998 TR alpha 1 and TR beta 2 each formed a single major TR : proteinTREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an oligomer .
TR alpha 1 and TR beta 2 each formed a single major TR : TREp complex which comigrated with the least retarded complex formed by GH3 NE , while TR beta 1 formed multiple complexes suggesting that it can bind to TREp as an proteinoligomer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7035 20.6364 10.9288 Interestingly, coincubation of 35S- TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly retarded complexes containing protein35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
3.6650 20.5181 10.7599 Interestingly, coincubation of protein35S- TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly retarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
2.3129 20.6035 0.9999 Interestingly, coincubation of 35S- TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the protein35S-TR: TREp complex , but in two additional more greatly retarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
1.3458 0.9997 10.9558 Interestingly, coincubation of 35S- proteinTR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly retarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
1.3276 0.9999 10.9012 Interestingly, coincubation of 35S- TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly retarded complexes containing 35S- proteinTR alpha 1 and comigrating with those formed by GH3 extract alone.
0.8246 1.0000 1.0000 Interestingly, coincubation of 35S- TR alpha 1 , GH3 NE , and unlabeled DNATREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly retarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
0.5345 1.0000 0.9860 Interestingly, coincubation of 35S- TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR: DNATREp complex , but in two additional more greatly retarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
1.2908 10.3021 0.9998 Interestingly, coincubation of 35S- TR alpha 1 , GH3 NE , and unlabeled TREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly proteinretarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
0.5903 0.9945 1.0000 Interestingly, coincubation of 35S- TR alpha 1 , proteinGH3 NE , and unlabeled TREp resulted in not only the 35S-TR: TREp complex , but in two additional more greatly retarded complexes containing 35S- TR alpha 1 and comigrating with those formed by GH3 extract alone.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6882 10.9392 0.9999 Incubation of each of the TRs with NE from cell_lineCOS-7 cells , which do not possess sufficient endogenous TRs to mediate T3-responses , resulted in formation of a new, more greatly shifted complex .
0.8674 1.0000 1.0000 Incubation of each of the TRs with NE from COS-7 cells , which do not possess sufficient endogenous proteinTRs to mediate T3-responses , resulted in formation of a new, more greatly shifted complex .
0.8557 0.9998 1.0000 Incubation of each of the proteinTRs with NE from COS-7 cells , which do not possess sufficient endogenous TRs to mediate T3-responses , resulted in formation of a new, more greatly shifted complex .
2.2345 20.4945 1.0000 Incubation of each of the TRs with NE from COS-7 cells , which do not possess sufficient proteinendogenous TRs to mediate T3-responses , resulted in formation of a new, more greatly shifted complex .
0.8349 0.9999 1.0000 Incubation of each of the TRs with proteinNE from COS-7 cells , which do not possess sufficient endogenous TRs to mediate T3-responses , resulted in formation of a new, more greatly shifted complex .
0.6601 0.9998 1.0000 Incubation of each of the TRs with NE from COS-7 cells , which do not possess sufficient endogenous TRs to mediate T3-responses , resulted in formation of a new, more greatly shifted proteincomplex .
Incubation of each of the TRs with NE from COS-7 cells , which do not possess sufficient endogenous TRs to mediate T3-responses , resulted in formation of a new, more proteingreatly shifted complex .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1258 10.8485 10.8617 A similar, heat labile activity which altered mobility of the TR:TRE complex was also present in NE from cell_lineT3-unresponsive JEG-3 cells .
2.1536 20.1374 1.0000 A similar, heat labile activity which altered mobility of the proteinTR:TRE complex was also present in NE from T3-unresponsive JEG-3 cells .
1.5559 10.4459 1.0000 A similar, heat labile activity which altered mobility of the TR:TRE complex was also present in proteinNE from T3-unresponsive JEG-3 cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8197 10.8047 1.0000 At high concentration of NE , all of the TR bound to DNATREp was more greatly retarded than in the absence of NE .
1.6897 10.9962 1.0000 At high concentration of NE , all of the proteinTR bound to TREp was more greatly retarded than in the absence of NE .
2.4028 20.0504 1.0000 At high concentration of proteinNE , all of the TR bound to TREp was more greatly retarded than in the absence of NE .
2.2471 20.4383 1.0000 At high concentration of NE , all of the TR bound to TREp was more greatly retarded than in the absence of proteinNE .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9284 20.9502 10.3765 Truncation of proteinTR alpha 1 at amino acid 210 prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the carboxyl-terminus of the TRs is essential for interaction with nuclear proteins .
2.3349 10.5029 10.6443 Truncation of TR alpha 1 at proteinamino acid 210 prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the carboxyl-terminus of the TRs is essential for interaction with nuclear proteins .
2.1481 20.6673 0.9999 Truncation of TR alpha 1 at amino acid 210 prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the carboxyl-terminus of the TRs is essential for interaction with proteinnuclear proteins .
1.5795 10.4350 1.0000 Truncation of TR alpha 1 at amino acid 210 prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the carboxyl-terminus of the proteinTRs is essential for interaction with nuclear proteins .
1.4909 10.7915 1.0000 Truncation of TR alpha 1 at amino acid 210 prevented additional complex formation in the presence of NE without affecting DNA binding , suggesting that the proteincarboxyl-terminus of the TRs is essential for interaction with nuclear proteins .
1.5505 10.2569 1.0000 Truncation of TR alpha 1 at amino acid 210 prevented additional complex formation in the presence of proteinNE without affecting DNA binding , suggesting that the carboxyl-terminus of the TRs is essential for interaction with nuclear proteins .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9808 20.7145 10.6722 Cell-specific differences in activation of DNANF-kappa B regulatory elements of human immunodeficiency virus and beta interferon promoters by tumor necrosis factor .
2.8385 20.7383 10.9818 Cell-specific differences in activation of NF-kappa B regulatory elements of human immunodeficiency virus and beta interferon promoters by proteintumor necrosis factor .
1.9436 20.8512 0.9705 Cell-specific differences in activation of proteinNF-kappa B regulatory elements of human immunodeficiency virus and beta interferon promoters by tumor necrosis factor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0478 20.4518 10.6667 Three aspects of the involvement of proteintumor necrosis factor in human immunodeficiency virus ( HIV ) pathogenesis were examined.
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1611 20.6452 20.8521 Tumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a cell_linechronically HIV infected U937 cell line ( U9-IIIB ).
4.0035 20.9615 10.9971 Tumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in cell_linemonocytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ).
1.6080 0.9494 10.3129 RNATumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ).
1.4430 0.9982 10.3031 proteinTumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ).
0.9629 1.0000 0.9991 Tumor necrosis factor alpha ( proteinTNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ).
0.8769 0.9999 1.0000 Tumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line ( cell_lineU9-IIIB ).
1.4318 0.9868 10.9727 Tumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected cell_lineU937 cell line ( U9-IIIB ).
0.7177 0.9641 0.9998 Tumor necrosis factor alpha ( RNATNF-alpha ) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line ( U9-IIIB ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2750 20.0437 0.9999 TNF-alpha RNA was undetectable in U937 cells , whereas a low constitutive level was detected in cell_lineU9-IIIB cells .
1.5062 10.9428 0.9999 TNF-alpha RNA was undetectable in cell_lineU937 cells , whereas a low constitutive level was detected in U9-IIIB cells .
0.9006 0.9982 1.0000 RNATNF-alpha RNA was undetectable in U937 cells , whereas a low constitutive level was detected in U9-IIIB cells .
0.8355 1.0000 0.9813 proteinTNF-alpha RNA was undetectable in U937 cells , whereas a low constitutive level was detected in U9-IIIB cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3465 20.8144 1.0000 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of RNATNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
2.0760 20.7605 0.9879 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of proteinTNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
1.6875 10.1713 1.0000 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that HIV-infected monocytic cells produced higher levels of proteinTNF-alpha than did normal cells after a secondary virus infection .
1.5877 10.8036 0.9999 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in cell_lineU9-IIIB cells compared with U937 cells , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
1.5352 10.7311 0.9999 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with cell_lineU937 cells , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
3.8796 20.9513 10.9828 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that cell_typeHIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
1.5624 10.3168 0.9999 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did cell_typenormal cells after a secondary virus infection .
1.2995 1.0000 10.2919 Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that HIV-infected cell_typemonocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells , suggesting that cell_lineHIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7070 20.7688 10.8778 The effects of TNF-alpha on gene expression were examined by transient expression assays using DNAreporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the HIV long terminal repeat ( LTR ) and the beta interferon promoter .
3.8355 20.8065 10.6167 The effects of TNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the DNAHIV long terminal repeat ( LTR ) and the beta interferon promoter .
3.5108 20.3525 10.8408 The effects of TNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the HIV long terminal repeat ( LTR ) and the DNAbeta interferon promoter .
2.1458 20.6895 1.0000 The effects of proteinTNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the HIV long terminal repeat ( LTR ) and the beta interferon promoter .
1.3463 10.7024 0.9999 The effects of TNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to DNAregulatory elements from the HIV long terminal repeat ( LTR ) and the beta interferon promoter .
0.9315 1.0000 1.0000 The effects of TNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the HIV long terminal repeat ( DNALTR ) and the beta interferon promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8748 30.0326 10.9961 In U937 and Jurkat T lymphoid cells , the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of DNANF-kappa B -containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .
2.1889 20.5619 1.0000 In U937 and Jurkat T lymphoid cells , the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of NF-kappa B -containing plasmids correlated directly with induction of proteinNF-kappa B DNA-binding activity .
2.0866 20.3425 0.9714 In U937 and Jurkat T lymphoid cells , the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of proteinNF-kappa B -containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .
1.4139 10.6690 0.9999 In U937 and Jurkat T lymphoid cells , the inducibility of the different DNAhybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of NF-kappa B -containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .
0.9039 1.0000 1.0000 In U937 and Jurkat T lymphoid cells , the inducibility of the different hybrid promoters by proteinTNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of NF-kappa B -containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .
3.2043 20.8067 10.4623 In U937 and cell_lineJurkat T lymphoid cells , the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of NF-kappa B -containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .
0.8872 0.9992 1.0000 In cell_lineU937 and Jurkat T lymphoid cells , the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of NF-kappa B -containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity .
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3.2506 30.9153 10.4441 Although the intact beta interferon promoter was only weakly stimulated by phorbol ester or TNF-alpha , multimers of the DNAPRDII NF-kappa B -binding domain were inducible by both agents.
2.4895 20.7038 10.5736 Although the intact DNAbeta interferon promoter was only weakly stimulated by phorbol ester or TNF-alpha , multimers of the PRDII NF-kappa B -binding domain were inducible by both agents.
1.4797 10.3830 1.0000 Although the intact beta interferon promoter was only weakly stimulated by phorbol ester or proteinTNF-alpha , multimers of the PRDII NF-kappa B -binding domain were inducible by both agents.
0.8540 1.0000 0.9685 Although the intact beta interferon promoter was only weakly stimulated by phorbol ester or TNF-alpha , multimers of the PRDII proteinNF-kappa B -binding domain were inducible by both agents.
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2.1835 20.3495 0.9999 TNF-alpha was able to increase expression of the HIV LTR in T cells , but in cell_typemonocytic cells , TNF-alpha did not induce the HIV LTR above a constitutive level of activity .
2.1689 20.8578 1.0000 TNF-alpha was able to increase expression of the HIV LTR in T cells , but in monocytic cells , TNF-alpha did not induce the DNAHIV LTR above a constitutive level of activity .
2.1613 20.7905 0.9999 TNF-alpha was able to increase expression of the DNAHIV LTR in T cells , but in monocytic cells , TNF-alpha did not induce the HIV LTR above a constitutive level of activity .
1.4628 10.8642 0.9998 TNF-alpha was able to increase expression of the HIV LTR in cell_typeT cells , but in monocytic cells , TNF-alpha did not induce the HIV LTR above a constitutive level of activity .
0.9817 1.0000 1.0000 proteinTNF-alpha was able to increase expression of the HIV LTR in T cells , but in monocytic cells , TNF-alpha did not induce the HIV LTR above a constitutive level of activity .
0.9491 1.0000 1.0000 TNF-alpha was able to increase expression of the HIV LTR in T cells , but in monocytic cells , proteinTNF-alpha did not induce the HIV LTR above a constitutive level of activity .
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2.6025 20.8567 1.0000 This level of NF-kappa B -independent activity appears to be sufficient for virus multiplication , since TNF-alpha treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infection and RNAviral RNA production in U937 cells .
2.5331 20.4056 1.0000 This level of proteinNF-kappa B -independent activity appears to be sufficient for virus multiplication , since TNF-alpha treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infection and viral RNA production in U937 cells .
2.4331 20.3431 0.9999 This level of NF-kappa B -independent activity appears to be sufficient for virus multiplication , since TNF-alpha treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infection and viral RNA production in cell_lineU937 cells .
0.9491 1.0000 1.0000 This level of NF-kappa B -independent activity appears to be sufficient for virus multiplication , since proteinTNF-alpha treatment had no effect on the kinetics of de novo HIV type 1 ( HIV-1 ) infection and viral RNA production in U937 cells .
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2.5309 20.1828 1.0000 However, in Jurkat cells , TNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased RNAviral RNA synthesis , indicating that in T cells HIV-1 multiplication was stimulated by TNF-alpha treatment .
2.4375 20.0528 0.9999 However, in cell_lineJurkat cells , TNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased viral RNA synthesis , indicating that in T cells HIV-1 multiplication was stimulated by TNF-alpha treatment .
2.3573 20.1657 0.9999 However, in Jurkat cells , TNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased viral RNA synthesis , indicating that in cell_typeT cells HIV-1 multiplication was stimulated by TNF-alpha treatment .
1.7304 10.1851 1.0000 However, in Jurkat cells , TNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased viral RNA synthesis , indicating that in T cells HIV-1 multiplication was stimulated by proteinTNF-alpha treatment .
0.9395 1.0000 1.0000 However, in Jurkat cells , proteinTNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased viral RNA synthesis , indicating that in T cells HIV-1 multiplication was stimulated by TNF-alpha treatment .
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3.4590 20.0159 10.7811 Functional analysis of cis-linked regulatory sequences in the DNAHLA DRA promoter by transcription in vitro.
3.4184 20.4203 10.6515 Functional analysis of DNAcis-linked regulatory sequences in the HLA DRA promoter by transcription in vitro.
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5.0513 20.4813 20.7040 Two consensus sequences, called X and Y boxes , capable of binding nuclear proteins and regulating expression in B cells have been defined within the immediate upstream region of DNAmajor histocompatibility complex (MHC) class II promoters .
2.0849 20.0567 0.9999 Two consensus sequences, called X and Y boxes , capable of binding nuclear proteins and regulating expression in cell_typeB cells have been defined within the immediate upstream region of major histocompatibility complex (MHC) class II promoters .
0.6866 0.9988 0.9999 Two consensus sequences, called X and Y boxes , capable of binding proteinnuclear proteins and regulating expression in B cells have been defined within the immediate upstream region of major histocompatibility complex (MHC) class II promoters .
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3.9120 20.5388 10.7119 Unlike other class II promoters , the DNAHLA-DR alpha (DRA) promoter also contains one element identical to the "octamer" motif of immunoglobulin variable region promoters that is responsible for B cell-specific transcription .
3.8309 20.0376 10.7306 Unlike other class II promoters , the HLA-DR alpha (DRA) promoter also contains one element identical to the "octamer" motif of DNAimmunoglobulin variable region promoters that is responsible for B cell-specific transcription .
3.7693 20.4306 10.9834 Unlike other DNAclass II promoters , the HLA-DR alpha (DRA) promoter also contains one element identical to the "octamer" motif of immunoglobulin variable region promoters that is responsible for B cell-specific transcription .
1.0709 10.8128 0.9998 Unlike other class II promoters , the HLA-DR alpha (DRA) promoter also contains one element identical to the DNA"octamer" motif of immunoglobulin variable region promoters that is responsible for B cell-specific transcription .
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2.2384 20.6990 0.9999 This " octamer " in the context of DRA appears capable of binding both the ubiquitous ( OTF-1 ) and lymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct protein"octamer" complex was found.
0.9767 1.0000 1.0000 This " octamer " in the context of DRA appears capable of binding both the ubiquitous ( proteinOTF-1 ) and lymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
0.9607 1.0000 1.0000 This " octamer " in the context of DRA appears capable of binding both the ubiquitous ( OTF-1 ) and lymphoid-specific ( proteinOTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
0.9220 1.0000 0.9995 This " DNAoctamer " in the context of DRA appears capable of binding both the ubiquitous ( OTF-1 ) and lymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
1.6044 10.1121 1.0000 This " octamer " in the context of DNADRA appears capable of binding both the ubiquitous ( OTF-1 ) and lymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
This " octamer " in the context of proteinDRA appears capable of binding both the ubiquitous ( OTF-1 ) and lymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
This " octamer " in the context of DRA appears capable of binding both the proteinubiquitous ( OTF-1 ) and lymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
This " octamer " in the context of DRA appears capable of binding both the ubiquitous ( OTF-1 ) and proteinlymphoid-specific ( OTF-2 ) "octamer" binding proteins , but at least one other distinct "octamer" complex was found.
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4.9543 20.8205 10.7081 In order to characterize the function of cis-acting elements , we have developed an in vitro system in which a DRA promoter construct is transcribed more efficiently in extracts from B cells than in extracts from cell_lineclass II-negative HeLa cells .
2.2611 20.9703 0.9999 In order to characterize the function of cis-acting elements , we have developed an in vitro system in which a DNADRA promoter construct is transcribed more efficiently in extracts from B cells than in extracts from class II-negative HeLa cells .
2.2299 20.5942 0.9999 In order to characterize the function of cis-acting elements , we have developed an in vitro system in which a DRA promoter construct is transcribed more efficiently in extracts from cell_typeB cells than in extracts from class II-negative HeLa cells .
2.1626 20.8387 1.0000 In order to characterize the function of DNAcis-acting elements , we have developed an in vitro system in which a DRA promoter construct is transcribed more efficiently in extracts from B cells than in extracts from class II-negative HeLa cells .
1.6280 20.8656 0.7477 In order to characterize the function of cis-acting elements , we have developed an in vitro system in which a DNADRA promoter construct is transcribed more efficiently in extracts from B cells than in extracts from class II-negative HeLa cells .
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2.2348 20.2914 0.9999 5' deletion constructs which lacked the Y box , but retained the DNA"octamer" motif and TATA box were completely inactive, and internal deletion of the Y box reduced transcription by 95%.
2.2221 20.5342 1.0000 5' deletion constructs which lacked the Y box , but retained the "octamer" motif and TATA box were completely inactive, and internal deletion of the DNAY box reduced transcription by 95%.
2.1688 20.2753 1.0000 5' deletion constructs which lacked the DNAY box , but retained the "octamer" motif and TATA box were completely inactive, and internal deletion of the Y box reduced transcription by 95%.
1.5364 10.5905 0.9999 5' deletion constructs which lacked the Y box , but retained the "octamer" motif and DNATATA box were completely inactive, and internal deletion of the Y box reduced transcription by 95%.
1.5528 0.9981 10.8279 DNA5' deletion constructs which lacked the Y box , but retained the "octamer" motif and TATA box were completely inactive, and internal deletion of the Y box reduced transcription by 95%.
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3.8591 20.6004 10.7849 Using supercoiled, but not linear templates, we observed differences in transcription efficiencies from templates lacking or disrupting the DNAX consensus element that reflect effects of random replacement of X box sequences in transient expression assays .
3.1017 20.8736 10.8700 Using supercoiled, but not linear templates, we observed differences in transcription efficiencies from templates lacking or disrupting the X consensus element that reflect effects of random replacement of DNAX box sequences in transient expression assays .
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2.2333 20.0906 1.0000 Demonstration of the complete dependence on the Y box in this system suggests that, despite its demonstrated importance in the DNADRA promoter , the DRA "octamer" does not utilize OTF-2 in a manner analogous to immunoglobulin promoters in B cells .
2.2257 20.1758 1.0000 Demonstration of the complete dependence on the DNAY box in this system suggests that, despite its demonstrated importance in the DRA promoter , the DRA "octamer" does not utilize OTF-2 in a manner analogous to immunoglobulin promoters in B cells .
2.2173 20.2810 0.9999 Demonstration of the complete dependence on the Y box in this system suggests that, despite its demonstrated importance in the DRA promoter , the DRA "octamer" does not utilize OTF-2 in a manner analogous to DNAimmunoglobulin promoters in B cells .
1.6419 10.3360 0.9997 Demonstration of the complete dependence on the Y box in this system suggests that, despite its demonstrated importance in the DRA promoter , the DRA "octamer" does not utilize OTF-2 in a manner analogous to immunoglobulin promoters in cell_typeB cells .
0.8365 1.0000 1.0000 Demonstration of the complete dependence on the Y box in this system suggests that, despite its demonstrated importance in the DRA promoter , the DRA "octamer" does not utilize proteinOTF-2 in a manner analogous to immunoglobulin promoters in B cells .
1.3141 10.7640 0.9995 Demonstration of the complete dependence on the Y box in this system suggests that, despite its demonstrated importance in the DRA promoter , the DNADRA "octamer" does not utilize OTF-2 in a manner analogous to immunoglobulin promoters in B cells .
Demonstration of the complete dependence on the Y box in this system suggests that, despite its demonstrated importance in the DRA promoter , the DNADRA "octamer" does not utilize OTF-2 in a manner analogous to immunoglobulin promoters in B cells .
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4.1049 30.2923 10.7185 Lipopolysaccharide ( LPS ) potently stimulates human immunodeficiency virus type 1-long terminal repeat ( HIV-1-LTR ) CAT constructs transfected into cell_linemonocyte/macrophage-like cell lines but not a T cell line .
3.5900 40.7147 20.8924 Lipopolysaccharide ( LPS ) potently stimulates DNAhuman immunodeficiency virus type 1-long terminal repeat ( HIV-1-LTR ) CAT constructs transfected into monocyte/macrophage-like cell lines but not a T cell line .
2.9170 20.2892 10.4406 Lipopolysaccharide ( LPS ) potently stimulates human immunodeficiency virus type 1-long terminal repeat ( HIV-1-LTR ) CAT constructs transfected into monocyte/macrophage-like cell lines but not a cell_lineT cell line .
2.3704 10.0251 20.3948 Lipopolysaccharide ( LPS ) potently stimulates DNAhuman immunodeficiency virus type 1-long terminal repeat ( HIV-1-LTR ) CAT constructs transfected into monocyte/macrophage-like cell lines but not a T cell line .
0.8664 1.0000 0.9799 Lipopolysaccharide ( LPS ) potently stimulates human immunodeficiency virus type 1-long terminal repeat ( DNAHIV-1-LTR ) CAT constructs transfected into monocyte/macrophage-like cell lines but not a T cell line .
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2.8540 10.7740 10.9322 This effect appears to be mediated through the induction of proteinnuclear factor kappa B ( NF-kappa B ).
0.8108 0.9998 0.9999 This effect appears to be mediated through the induction of nuclear factor kappa B ( proteinNF-kappa B ).
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1.5957 10.1248 0.9997 Electrophoretic mobility shift assays demonstrate that LPS induces a DNA binding activity indistinguishable from NF-kappa B in U937 and cell_lineTHP-1 cells .
1.5756 10.9743 1.0000 Electrophoretic mobility shift assays demonstrate that LPS induces a DNA binding activity indistinguishable from proteinNF-kappa B in U937 and THP-1 cells .
0.9018 0.9998 1.0000 Electrophoretic mobility shift assays demonstrate that LPS induces a DNA binding activity indistinguishable from NF-kappa B in cell_lineU937 and THP-1 cells .
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6.4981 30.9065 20.4155 LPS is also shown to dramatically increase HIV-1 production from a cell_linechronically infected monocyte/macrophage-like cloned cell line , U1 , which produces very low levels of HIV-1 at baseline.
0.9313 0.9999 1.0000 LPS is also shown to dramatically increase HIV-1 production from a chronically infected monocyte/macrophage-like cloned cell line , cell_lineU1 , which produces very low levels of HIV-1 at baseline.
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3.7743 20.6391 10.3173 The stimulation of viral production from this cell line occurs only if these cells are treated with proteingranulocyte/macrophage colony-stimulating factor ( GM-CSF ) before treatment with LPS .
0.9740 1.0000 1.0000 The stimulation of viral production from this cell line occurs only if these cells are treated with granulocyte/macrophage colony-stimulating factor ( proteinGM-CSF ) before treatment with LPS .
2.1682 20.2160 0.9999 The stimulation of viral production from this cell_linecell line occurs only if these cells are treated with granulocyte/macrophage colony-stimulating factor ( GM-CSF ) before treatment with LPS .
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1.7353 10.8801 1.0000 This stimulation of HIV-1 production is correlated with an increase in the level of RNAHIV-1 RNA and and activation of NF-kappa B .
1.5699 10.9735 1.0000 This stimulation of HIV-1 production is correlated with an increase in the level of HIV-1 RNA and and activation of proteinNF-kappa B .
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3.9927 20.5853 10.6203 LPS is not able to induce HIV-1 production in a cell_linecloned T cell line .
LPS is not able to induce HIV-1 production in a cloned cell_lineT cell line .
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2.5075 20.3224 1.0000 The suppression of cell_typebasophils measured as whole blood histamine and plasma cortisol concentrations was assessed during 32 hours.
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1.6498 10.7203 0.9999 A pharmacodynamic model for cell_typebasophil cell distribution to and from an extravascular compartment describes the effects of MP after both regimens.
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2.4563 20.7414 1.0000 A slower initial decline in blood histamine after the divided regimen may be related to incomplete suppression of cell_typebasophil cell return to blood .
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1.5724 10.8534 0.9999 1,25(OH)2D2 production by T lymphocytes and cell_typealveolar macrophages recovered by lavage from normocalcemic patients with tuberculosis.
1.4824 10.8130 0.9998 1,25(OH)2D2 production by cell_typeT lymphocytes and alveolar macrophages recovered by lavage from normocalcemic patients with tuberculosis.
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4.2022 20.9224 10.4144 To compare extra-renal 1,25(OH)2D3 production in different types of granulomatous disease , and to identify the cell types responsible, we have evaluated the conversion of 25(OH)D3 in 1,25(OH)2D3 by uncultured cells recovered by bronchoalveolar lavage and cell_typeblood mononuclear cells from normocalcemic patients with sarcoidosis and tuberculosis.
1.6762 10.9056 0.9999 To compare extra-renal 1,25(OH)2D3 production in different types of granulomatous disease , and to identify the cell types responsible, we have evaluated the conversion of 25(OH)D3 in 1,25(OH)2D3 by cell_typeuncultured cells recovered by bronchoalveolar lavage and blood mononuclear cells from normocalcemic patients with sarcoidosis and tuberculosis.
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3.9760 20.6807 10.5607 1,25(OH)2D3 was produced both by lavage cells (12/12 tuberculosis patients , 2/6 sarcoidosis patients ) and cell_typeblood mononuclear cells (3/5 tuberculosis patients , 0/3 sarcoidosis patients ) from patients but not controls, but significantly greater amounts were produced by lavage cells from tuberculosis patients than those of sarcoidosis patients (P less than 0.001).
2.4359 20.7636 0.9999 1,25(OH)2D3 was produced both by cell_typelavage cells (12/12 tuberculosis patients , 2/6 sarcoidosis patients ) and blood mononuclear cells (3/5 tuberculosis patients , 0/3 sarcoidosis patients ) from patients but not controls, but significantly greater amounts were produced by lavage cells from tuberculosis patients than those of sarcoidosis patients (P less than 0.001).
2.4120 20.5896 1.0000 1,25(OH)2D3 was produced both by lavage cells (12/12 tuberculosis patients , 2/6 sarcoidosis patients ) and blood mononuclear cells (3/5 tuberculosis patients , 0/3 sarcoidosis patients ) from patients but not controls, but significantly greater amounts were produced by cell_typelavage cells from tuberculosis patients than those of sarcoidosis patients (P less than 0.001).
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1.5192 10.7653 0.9999 1,25(OH)2D3 production by cell_typelavage cells from tuberculosis patients correlated with the number of CD8+ T lymphocytes present but not other cell types.
2.9919 10.8478 10.8604 1,25(OH)2D3 production by lavage cells from tuberculosis patients correlated with the number of cell_typeCD8+ T lymphocytes present but not other cell types.
1,25(OH)2D3 production by lavage cells from tuberculosis patients correlated with the number of CD8+ cell_typeT lymphocytes present but not other cell types.
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2.5759 20.2030 10.5585 T lymphocytes appeared to be an important source of 1,25(OH)2D3 production , since purified cell_typeT lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3 , and 1,25(OH)2D3 production by these cells correlated closely with that produced by unseparated lavage cells .
0.8749 0.9989 0.9999 cell_typeT lymphocytes appeared to be an important source of 1,25(OH)2D3 production , since purified T lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3 , and 1,25(OH)2D3 production by these cells correlated closely with that produced by unseparated lavage cells .
4.4759 30.0689 10.7917 T lymphocytes appeared to be an important source of 1,25(OH)2D3 production , since purified T lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3 , and 1,25(OH)2D3 production by these cells correlated closely with that produced by cell_typeunseparated lavage cells .
1.4376 20.9812 10.7442 T lymphocytes appeared to be an important source of 1,25(OH)2D3 production , since cell_typepurified T lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3 , and 1,25(OH)2D3 production by these cells correlated closely with that produced by unseparated lavage cells .
T lymphocytes appeared to be an important source of 1,25(OH)2D3 production , since purified T lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3 , and 1,25(OH)2D3 production by these cells correlated closely with that produced by unseparated cell_typelavage cells .
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1.7795 10.3376 1.0000 Because 1,25(OH)2D3 can improve the capacity of cell_typemacrophages to kill mycobacteria , our results support the conclusion that macrophage-lymphocyte interactions , mediated at least in part by 1,25(OH)2D3 , may be an important component of a successful antituberculous immune response .
0.7995 1.0000 1.0000 Because 1,25(OH)2D3 can improve the capacity of macrophages to kill mycobacteria , our results support the conclusion that cell_typemacrophage-lymphocyte interactions , mediated at least in part by 1,25(OH)2D3 , may be an important component of a successful antituberculous immune response .
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1.4438 10.7272 0.9998 Megakaryocytic and erythrocytic lineages share specific proteintranscription factors .
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2.1110 20.3901 0.9996 Erythroid-specific genes contain binding sites for NF-E1 (also called GF-1 and Eryf-1 ; refs 1-3 respectively), the principal DNA-binding protein of the cell_typeerythrocytic lineage .
2.1082 20.5331 1.0000 Erythroid-specific genes contain binding sites for NF-E1 (also called GF-1 and Eryf-1 ; refs 1-3 respectively), the principal proteinDNA-binding protein of the erythrocytic lineage .
1.7605 10.1080 1.0000 Erythroid-specific genes contain binding sites for NF-E1 (also called proteinGF-1 and Eryf-1 ; refs 1-3 respectively), the principal DNA-binding protein of the erythrocytic lineage .
1.4996 0.9990 10.3009 DNAErythroid-specific genes contain binding sites for NF-E1 (also called GF-1 and Eryf-1 ; refs 1-3 respectively), the principal DNA-binding protein of the erythrocytic lineage .
0.9163 1.0000 1.0000 Erythroid-specific genes contain binding sites for proteinNF-E1 (also called GF-1 and Eryf-1 ; refs 1-3 respectively), the principal DNA-binding protein of the erythrocytic lineage .
0.8936 1.0000 1.0000 Erythroid-specific genes contain binding sites for NF-E1 (also called GF-1 and proteinEryf-1 ; refs 1-3 respectively), the principal DNA-binding protein of the erythrocytic lineage .
1.3861 10.5673 0.9999 Erythroid-specific genes contain DNAbinding sites for NF-E1 (also called GF-1 and Eryf-1 ; refs 1-3 respectively), the principal DNA-binding protein of the erythrocytic lineage .
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2.0035 20.9796 0.9998 NF-E1 expression seems to be restricted to the cell_typeerythrocytic lineage .
0.9690 1.0000 1.0000 proteinNF-E1 expression seems to be restricted to the erythrocytic lineage .
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4.7321 20.3901 10.9059 A closely related (if not identical) protein is found in both a cell_linehuman megakaryocytic cell line and purified human megakaryocytes ; it binds to promoter regions of two megakaryocytic-specific genes .
3.0493 10.8966 10.7888 A closely related (if not identical) protein is found in both a human megakaryocytic cell line and cell_linepurified human megakaryocytes ; it binds to promoter regions of two megakaryocytic-specific genes .
1.4149 10.7752 0.9999 A closely related (if not identical) protein is found in both a human megakaryocytic cell line and purified human megakaryocytes ; it binds to DNApromoter regions of two megakaryocytic-specific genes .
1.3761 10.7032 0.9997 A closely related (if not identical) protein is found in both a human megakaryocytic cell line and purified human megakaryocytes ; it binds to promoter regions of two DNAmegakaryocytic-specific genes .
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2.6141 20.3457 0.9999 The binding sites and partial proteolysis profile of this protein are indistinguishable from those of the erythroid protein ; also, RNANF-E1 messenger RNA is the same size in both the megakaryocytic and erythroid cell lines .
1.5947 10.9736 1.0000 The binding sites and partial proteolysis profile of this protein are indistinguishable from those of the proteinerythroid protein ; also, NF-E1 messenger RNA is the same size in both the megakaryocytic and erythroid cell lines .
1.5301 10.8847 0.9990 The binding sites and partial proteolysis profile of this protein are indistinguishable from those of the erythroid protein ; also, proteinNF-E1 messenger RNA is the same size in both the megakaryocytic and erythroid cell lines .
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2.3361 20.3911 1.0000 Furthermore, point mutations that abolish binding of NF-E1 result in a 70% decrease in the transcriptional activity of a DNAmegakaryocytic-specific promoter .
1.6058 10.6285 1.0000 Furthermore, point mutations that abolish binding of proteinNF-E1 result in a 70% decrease in the transcriptional activity of a megakaryocytic-specific promoter .
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2.2153 20.0269 0.9999 We also find that NF-E2 , another trans-acting factor of the cell_typeerythrocytic lineage , is present in megakaryocytes .
2.0719 20.2233 0.9999 We also find that NF-E2 , another proteintrans-acting factor of the erythrocytic lineage , is present in megakaryocytes .
1.5489 10.8192 0.9999 We also find that NF-E2 , another trans-acting factor of the erythrocytic lineage , is present in cell_linemegakaryocytes .
1.5112 10.8735 1.0000 We also find that proteinNF-E2 , another trans-acting factor of the erythrocytic lineage , is present in megakaryocytes .
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2.3231 20.4876 1.0000 Transcriptional effects in both lineages might then be mediated in part by the same specific proteintrans-acting factors .
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5.4041 30.9917 10.9404 Our data strengthen the idea of a close association between the erythrocytic and the megakaryocytic lineages and could also explain the expression of markers specific to the erythrocytic and megakaryocytic lineages in most cell_lineerythroblastic and megakaryoblastic permanent cell lines .
2.5279 20.2556 0.9911 Our data strengthen the idea of a close association between the erythrocytic and the megakaryocytic lineages and could also explain the expression of markers specific to the erythrocytic and megakaryocytic lineages in most cell_lineerythroblastic and megakaryoblastic permanent cell lines .
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6.3852 40.1206 20.4501 Transcriptional down-regulation of c-myc expression by protein synthesis -dependent and -independent pathways in a cell_linehuman T lymphoblastic tumor cell line .
2.1035 20.9251 1.0000 Transcriptional down-regulation of DNAc-myc expression by protein synthesis -dependent and -independent pathways in a human T lymphoblastic tumor cell line .
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3.9770 40.8201 10.9613 We show that in the cell_linehuman T lymphoblastic tumor cell line Molt4 c-myc mRNA and protein expression is down-regulated after exposure to dimethyl sulfoxide , to phorbol myristate acetate , or to the calcium ionophore A23187 , which raises the intracellular calcium concentration .
2.2708 10.1575 10.7168 We show that in the human T lymphoblastic tumor cell line RNAMolt4 c-myc mRNA and protein expression is down-regulated after exposure to dimethyl sulfoxide , to phorbol myristate acetate , or to the calcium ionophore A23187 , which raises the intracellular calcium concentration .
1.1705 0.9999 10.0344 We show that in the human T lymphoblastic tumor cell line Molt4 RNAc-myc mRNA and protein expression is down-regulated after exposure to dimethyl sulfoxide , to phorbol myristate acetate , or to the calcium ionophore A23187 , which raises the intracellular calcium concentration .
We show that in the human T lymphoblastic tumor cell line Molt4 DNAc-myc mRNA and protein expression is down-regulated after exposure to dimethyl sulfoxide , to phorbol myristate acetate , or to the calcium ionophore A23187 , which raises the intracellular calcium concentration .
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1.7343 10.4761 1.0000 A block to RNA elongation is largely responsible for decreased DNAc-myc transcription .
1.0901 10.1449 1.0000 A block to RNARNA elongation is largely responsible for decreased c-myc transcription .
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1.8088 10.3556 1.0000 The calcium ionophore-induced DNAc-myc suppression , however, strictly requires de novo protein synthesis .
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1.8164 10.6164 1.0000 Therefore, two different negative regulatory pathways are involved in DNAc-myc regulation : one which is independent and one which depends on de novo protein synthesis .
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2.0993 10.1897 20.2073 The latter one appears to be mediated by a rapidly proteincalcium -dependent induced gene product .
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0.9868 1.0000 1.0000 Oestrogen receptor ( proteinER ) analysis in B-cell chronic lymphocytic leukemia : correlation of biochemical and immunocytochemical methods .
0.9127 0.9995 1.0000 proteinOestrogen receptor ( ER ) analysis in B-cell chronic lymphocytic leukemia : correlation of biochemical and immunocytochemical methods .
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3.7104 20.4252 10.4474 Oestrogen receptors ( ER ) are present in cell_typeneoplastic lymphoid cells and have been considered a physiological marker of growth rate or differentiation.
0.9774 1.0000 1.0000 Oestrogen receptors ( proteinER ) are present in neoplastic lymphoid cells and have been considered a physiological marker of growth rate or differentiation.
0.8775 0.9992 1.0000 proteinOestrogen receptors ( ER ) are present in neoplastic lymphoid cells and have been considered a physiological marker of growth rate or differentiation.
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1.8619 10.7319 1.0000 Until now, proteinER status has been assessed using a steroid binding assay ( SBA ) which has many inherent problems.
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1.8297 10.3127 1.0000 Recently, the development of monoclonal antibodies directed against proteinER has been applied to the study of breast carcinomas and results obtained show good correlation with the quantitative SBA .
2.5298 20.4952 1.0000 Recently, the development of proteinmonoclonal antibodies directed against ER has been applied to the study of breast carcinomas and results obtained show good correlation with the quantitative SBA .
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1.4703 10.1450 0.9998 In 30 of these cases ER enzyme immunoassay ( proteinER -EIA ) was also performed.
0.5429 0.9997 1.0000 In 30 of these cases ER enzyme immunoassay ( proteinER -EIA ) was also performed.
In 30 of these cases proteinER enzyme immunoassay ( ER -EIA ) was also performed.
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3.4645 20.8224 10.6562 Cultured MCF-7 cells , derived from a pleural effusion of a breast cancer patient , known to contain high levels of ER were used as a positive control (40-48% cell_typeER positive cells by immunocytochemistry; 200 fmol/mg protein by EIA).
1.7282 0.9987 10.7322 cell_lineCultured MCF-7 cells , derived from a pleural effusion of a breast cancer patient , known to contain high levels of ER were used as a positive control (40-48% ER positive cells by immunocytochemistry; 200 fmol/mg protein by EIA).
1.7110 10.1990 1.0000 Cultured MCF-7 cells , derived from a pleural effusion of a breast cancer patient , known to contain high levels of proteinER were used as a positive control (40-48% ER positive cells by immunocytochemistry; 200 fmol/mg protein by EIA).
1.6487 10.6102 0.9951 Cultured MCF-7 cells , derived from a pleural effusion of a breast cancer patient , known to contain high levels of ER were used as a positive control (40-48% proteinER positive cells by immunocytochemistry; 200 fmol/mg protein by EIA).
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1.8208 10.5113 1.0000 All of the CLL cases except two (96%) were negative for proteinER (less than 1% staining; less than 4 fmol/mg protein).
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0.9389 1.0000 1.0000 The two positive cases expressed granular proteinER staining over the nucleus (9.2 and 12.1% positive cells) and were positive by EIA and SBA .
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1.7549 10.3157 1.0000 It is concluded that (i) patients with CLL rarely express proteinER and (ii) immunocytochemical staining of cytospin preparations is a valid technique for the measurement of ER .
1.7013 10.7121 1.0000 It is concluded that (i) patients with CLL rarely express ER and (ii) immunocytochemical staining of cytospin preparations is a valid technique for the measurement of proteinER .
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3.9845 30.3261 10.5819 Type-II estrogen binding sites in a cell_linelymphoblastoid cell line and growth-inhibitory effect of estrogen , anti-estrogen and bioflavonoids .
1.6171 0.9974 10.5170 proteinType-II estrogen binding sites in a lymphoblastoid cell line and growth-inhibitory effect of estrogen , anti-estrogen and bioflavonoids .
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1.5086 0.9971 10.0639 proteinType-II estrogen -binding sites ( type-II EBS ) have been demonstrated in the human lymphoblastoid cell line IM-9 using a whole-cell assay with (6,7-3H) estradiol ( 3H-E2 ) as tracer.
1.4651 10.3773 1.0000 Type-II estrogen -binding sites ( proteintype-II EBS ) have been demonstrated in the human lymphoblastoid cell line IM-9 using a whole-cell assay with (6,7-3H) estradiol ( 3H-E2 ) as tracer.
7.1012 30.7601 20.8467 Type-II estrogen -binding sites ( type-II EBS ) have been demonstrated in the cell_linehuman lymphoblastoid cell line IM-9 using a whole-cell assay with (6,7-3H) estradiol ( 3H-E2 ) as tracer.
Type-II estrogen -binding sites ( type-II EBS ) have been demonstrated in the human cell_linelymphoblastoid cell line IM-9 using a whole-cell assay with (6,7-3H) estradiol ( 3H-E2 ) as tracer.
Type-II estrogen -binding sites ( type-II EBS ) have been demonstrated in the human lymphoblastoid cell line cell_lineIM-9 using a whole-cell assay with (6,7-3H) estradiol ( 3H-E2 ) as tracer.
Type-II estrogen -binding sites ( type-II EBS ) have been demonstrated in the cell_linehuman lymphoblastoid cell line IM-9 using a whole-cell assay with (6,7-3H) estradiol ( 3H-E2 ) as tracer.
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1.5300 10.7695 0.9999 Competition analysis showed that the anti-estrogen tamoxifen and the flavonoids quercetin and rutin competed for (3H)-E2 binding to DNAtype-II EBS .
0.8303 1.0000 1.0000 Competition analysis showed that the anti-estrogen tamoxifen and the flavonoids quercetin and rutin competed for (3H)-E2 binding to type-II DNAEBS .
Competition analysis showed that the anti-estrogen tamoxifen and the flavonoids quercetin and rutin competed for (3H)-E2 binding to proteintype-II EBS .
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1.7734 20.9392 1.0000 The relative binding affinity of quercetin , rutin , DES and TAM for DNAtype-II EBS correlated well with their potency as cell growth inhibitors .
0.5376 1.0000 1.0000 The relative binding affinity of quercetin , rutin , DES and TAM for type-II DNAEBS correlated well with their potency as cell growth inhibitors .
The relative binding affinity of quercetin , rutin , DES and TAM for proteintype-II EBS correlated well with their potency as cell growth inhibitors .
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2.2237 20.8084 1.0000 Moreover, hesperidin, a flavonoid which does not bind to DNAtype-II EBS , was ineffective in inhibiting cell growth .
0.9568 1.0000 1.0000 Moreover, hesperidin, a flavonoid which does not bind to type-II DNAEBS , was ineffective in inhibiting cell growth .
Moreover, hesperidin, a flavonoid which does not bind to proteintype-II EBS , was ineffective in inhibiting cell growth .
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1.6554 10.9137 0.9999 Our results suggest that high estrogen and anti-estrogen concentrations and flavonoids may regulate cell_lineIM-9 cell growth through a common mechanism involving a binding interaction with type-II EBS .
Our results suggest that high estrogen and anti-estrogen concentrations and flavonoids may regulate cell_lineIM-9 cell growth through a common mechanism involving a binding interaction with type-II EBS .
Our results suggest that high estrogen and anti-estrogen concentrations and flavonoids may regulate IM-9 cell growth through a common mechanism involving a binding interaction with proteintype-II EBS .
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2.2023 10.8709 10.5047 [ Glucocorticoid receptors in cell_typeperipheral blood lymphocytes of patients with bronchial asthma ]
1.5233 10.3329 0.9999 [ proteinGlucocorticoid receptors in peripheral blood lymphocytes of patients with bronchial asthma ]
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4.0228 20.9290 10.7917 Quantitation of glucocorticoid receptors ( GCR ) and the study of their affinity for glucocorticosteroids ( GCS ) were made in cell_typeperipheral blood lymphocytes of bronchial asthma ( BA ) patients in consideration of GCR treatment and serum levels of endogenous cortisol .
2.3547 20.5809 1.0000 Quantitation of proteinglucocorticoid receptors ( GCR ) and the study of their affinity for glucocorticosteroids ( GCS ) were made in peripheral blood lymphocytes of bronchial asthma ( BA ) patients in consideration of GCR treatment and serum levels of endogenous cortisol .
1.7889 10.0622 1.0000 Quantitation of glucocorticoid receptors ( GCR ) and the study of their affinity for glucocorticosteroids ( GCS ) were made in peripheral blood lymphocytes of bronchial asthma ( BA ) patients in consideration of proteinGCR treatment and serum levels of endogenous cortisol .
0.9585 1.0000 1.0000 Quantitation of glucocorticoid receptors ( proteinGCR ) and the study of their affinity for glucocorticosteroids ( GCS ) were made in peripheral blood lymphocytes of bronchial asthma ( BA ) patients in consideration of GCR treatment and serum levels of endogenous cortisol .
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1.7279 10.2900 1.0000 It is stated that proteinGCR of healthy controls and GCS -untreated patients outnumbered those of cortisol-dependent BA patients on hormone therapy .
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0.9462 1.0000 1.0000 Following discontinuation of glucocorticoid drugs proteinGCR count in cortisol -dependent BA tends to rise.
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1.6714 10.3697 1.0000 Endogenous cortisol has no effect on proteinGCR level estimated by 3H-triamcinolone acetonide .
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2.4709 10.8609 10.3209 Two proteinglucocorticoid binding sites on the human glucocorticoid receptor .
2.4468 10.9405 10.4753 Two glucocorticoid binding sites on the proteinhuman glucocorticoid receptor .
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1.4802 10.8721 0.9999 Glucocorticoids are known to have a lytic effect in cell_typeleukemic cells via interactions with the glucocorticoid receptor ( GR ).
1.4559 10.8781 1.0000 Glucocorticoids are known to have a lytic effect in leukemic cells via interactions with the proteinglucocorticoid receptor ( GR ).
0.9544 1.0000 1.0000 Glucocorticoids are known to have a lytic effect in leukemic cells via interactions with the glucocorticoid receptor ( proteinGR ).
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1.7209 10.4472 1.0000 Cortisol and various synthetic glucocorticoids bind to the proteinGR with one-site kinetics .
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2.5535 20.6458 10.1656 Cortivazol ( CVZ ) is a unique, high potency synthetic glucocorticoid , which has a phenylpyrazol fused to the A-ring of the steroid nucleus and displays binding consistent with two or more sites in the cytosol from CEM C7 cells (a cell_linehuman acute lymphoblastic T-cell line ).
2.1554 20.4274 10.5657 Cortivazol ( CVZ ) is a unique, high potency synthetic glucocorticoid , which has a phenylpyrazol fused to the A-ring of the steroid nucleus and displays binding consistent with two or more sites in the cytosol from cell_lineCEM C7 cells (a human acute lymphoblastic T-cell line ).
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0.4805 0.9999 1.0000 It has previously been shown that the lower affinity class of DNAsites are similar in affinity and site molarity to those recognized by dexamethasone .
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2.3487 10.7703 10.2326 The proteinhigher affinity sites bind CVZ with 20- to 50-fold greater affinity , consistent with CVZ 's enhanced biological effects .
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3.8061 20.2001 10.6484 In mutant leukemic cells resistant to the lytic effects of dexamethasone , CVZ both lyses the cells and recognizes a single class of sites similar to the high affinity site in cell_lineCEM C7 cells .
4.3719 20.7891 10.9702 In mutant leukemic cells resistant to the lytic effects of dexamethasone , CVZ both lyses the cells and recognizes a single class of sites similar to the DNAhigh affinity site in CEM C7 cells .
2.2869 10.9013 10.0783 In cell_linemutant leukemic cells resistant to the lytic effects of dexamethasone , CVZ both lyses the cells and recognizes a single class of sites similar to the high affinity site in CEM C7 cells .
In mutant cell_typeleukemic cells resistant to the lytic effects of dexamethasone , CVZ both lyses the cells and recognizes a single class of sites similar to the high affinity site in CEM C7 cells .
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5.5370 30.3372 20.6201 We have carried out experiments to define the nature of the DNAhigher affinity CVZ binding site .
0.7909 1.0000 0.9800 We have carried out experiments to define the nature of the higher affinity proteinCVZ binding site .
We have carried out experiments to define the nature of the proteinhigher affinity CVZ binding site .
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2.4132 20.8115 0.9998 We now show that: 1) CVZ has more than one binding site in a second, independent, cell_lineB-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
0.9566 1.0000 1.0000 We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , cell_lineIM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
2.3829 20.9520 1.0000 We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the proteinhuman GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
2.1436 20.2756 1.0000 We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's DNAbinding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
1.7198 30.6502 0.9999 We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of cell_lineCVZ -resistant cells have lost all binding sites for CVZ .
1.5093 20.7872 0.9999 We now show that: 1) CVZ has more than one DNAbinding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
1.4357 30.7434 1.0000 We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all DNAbinding sites for CVZ .
We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of CVZ 's binding sites are on a protein immunologically indistinguishable from the human proteinGR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
We now show that: 1) CVZ has more than one binding site in a second, independent, B-cell line , IM-9 ; 2) the antiglucocorticoid RU 38486 is able to block both CVZ 's higher and lower affinity sites; 3) all of proteinCVZ 's binding sites are on a protein immunologically indistinguishable from the human GR ; and 4) freshly isolated clones of CVZ -resistant cells have lost all binding sites for CVZ .
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2.6604 10.6243 10.6650 These data indicate that CVZ is recognizing two DNAglucocorticoid binding sites on the human GR or a protein very similar to it.
1.5290 10.2364 1.0000 These data indicate that CVZ is recognizing two glucocorticoid binding sites on the proteinhuman GR or a protein very similar to it.
These data indicate that CVZ is recognizing two glucocorticoid binding sites on the human proteinGR or a protein very similar to it.
These data indicate that CVZ is recognizing two proteinglucocorticoid binding sites on the human GR or a protein very similar to it.
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2.9999 10.4534 10.5885 Retroviral mediated transfer and expression of exogenous genes in cell_typeprimary lymphoid cells : assaying for a viral transactivator activity in normal and malignant cells .
2.1652 20.5324 0.9999 Retroviral mediated transfer and expression of DNAexogenous genes in primary lymphoid cells : assaying for a viral transactivator activity in normal and malignant cells .
2.2050 20.1569 1.0000 Retroviral mediated transfer and expression of exogenous genes in primary lymphoid cells : assaying for a proteinviral transactivator activity in normal and malignant cells .
Retroviral mediated transfer and expression of exogenous genes in primary lymphoid cells : assaying for a viral proteintransactivator activity in normal and malignant cells .
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2.3789 20.3098 0.9999 In this report we describe the use of recombinant retroviruses to characterize the activity of an DNAexogenous promoter in primary cells obtained from patients with lymphoproliferative disorders .
1.6514 10.6169 0.9999 In this report we describe the use of recombinant retroviruses to characterize the activity of an exogenous promoter in cell_typeprimary cells obtained from patients with lymphoproliferative disorders .
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5.1955 30.2649 10.5756 The infection of a variety of cultured and primary lymphoid cells with a recombinant retrovirus containing a DNAhistone promoter-driven beta-galactosidase gene is shown to result in the expression of beta-galactosidase in 50% to 100% of the cells.
2.5514 20.7471 10.7049 The infection of a variety of cultured and cell_typeprimary lymphoid cells with a recombinant retrovirus containing a histone promoter-driven beta-galactosidase gene is shown to result in the expression of beta-galactosidase in 50% to 100% of the cells.
1.6549 10.2455 1.0000 The infection of a variety of cultured and primary lymphoid cells with a recombinant retrovirus containing a histone promoter-driven beta-galactosidase gene is shown to result in the expression of proteinbeta-galactosidase in 50% to 100% of the cells.
0.9459 1.0000 0.9942 The infection of a variety of cultured and primary lymphoid cells with a recombinant retrovirus containing a histone promoter-driven proteinbeta-galactosidase gene is shown to result in the expression of beta-galactosidase in 50% to 100% of the cells.
The infection of a variety of cultured and primary lymphoid cells with a recombinant retrovirus containing a proteinhistone promoter-driven beta-galactosidase gene is shown to result in the expression of beta-galactosidase in 50% to 100% of the cells.
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3.7981 20.2875 10.6756 A similar infection with a recombinant retrovirus containing the beta-galactosidase gene with an DNAadenovirus E2 promoter , results in beta-galactosidase activity in a limited number of cultured and primary cells .
2.2161 20.4392 1.0000 A similar infection with a recombinant retrovirus containing the DNAbeta-galactosidase gene with an adenovirus E2 promoter , results in beta-galactosidase activity in a limited number of cultured and primary cells .
2.1101 20.3863 0.9885 A similar infection with a recombinant retrovirus containing the proteinbeta-galactosidase gene with an adenovirus E2 promoter , results in beta-galactosidase activity in a limited number of cultured and primary cells .
0.9315 1.0000 1.0000 A similar infection with a recombinant retrovirus containing the beta-galactosidase gene with an adenovirus E2 promoter , results in proteinbeta-galactosidase activity in a limited number of cultured and primary cells .
A similar infection with a recombinant retrovirus containing the beta-galactosidase gene with an adenovirus E2 promoter , results in beta-galactosidase activity in a limited number of cell_linecultured and primary cells .
A similar infection with a recombinant retrovirus containing the beta-galactosidase gene with an adenovirus E2 promoter , results in beta-galactosidase activity in a limited number of cultured and cell_typeprimary cells .
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4.8732 30.0271 10.6495 Since the adenovirus E2 promoter has been well characterized and is known to be regulated by transactivators encoded by many viruses , the activity of this promoter in specific cell types is discussed in reference to both the biology of the cell and the possible presence of as yet undetected proteinviral gene products .
2.3367 20.7751 10.4161 Since the DNAadenovirus E2 promoter has been well characterized and is known to be regulated by transactivators encoded by many viruses , the activity of this promoter in specific cell types is discussed in reference to both the biology of the cell and the possible presence of as yet undetected viral gene products .
1.6793 10.2081 1.0000 Since the adenovirus E2 promoter has been well characterized and is known to be regulated by proteintransactivators encoded by many viruses , the activity of this promoter in specific cell types is discussed in reference to both the biology of the cell and the possible presence of as yet undetected viral gene products .
0.8230 1.0000 1.0000 Since the adenovirus E2 promoter has been well characterized and is known to be regulated by transactivators encoded by many viruses , the activity of this DNApromoter in specific cell types is discussed in reference to both the biology of the cell and the possible presence of as yet undetected viral gene products .
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1.8110 10.6545 1.0000 Concentration of receptors of hormonal form of 1,25(OH)2D3 was found to be minimal in cell_typelymphocytes under conditions of chronic kidney insufficiency , while their expression, after the dioxyvit action, was detected only in patients with glomerulonephritis .
1.7380 10.7048 1.0000 Concentration of proteinreceptors of hormonal form of 1,25(OH)2D3 was found to be minimal in lymphocytes under conditions of chronic kidney insufficiency , while their expression, after the dioxyvit action, was detected only in patients with glomerulonephritis .
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1.6033 10.6049 1.0000 [The role of glucocorticoid receptors and proteinHLA antigens in the pathogenesis of Cushing's syndrome ]
1.4745 10.9862 1.0000 [The role of proteinglucocorticoid receptors and HLA antigens in the pathogenesis of Cushing's syndrome ]
[The role of glucocorticoid receptors and HLA antigens in the pathogenesis of proteinCushing's syndrome ]
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1.6368 10.7093 1.0000 Lymphocytic levels of proteinglucocorticoid receptors were evaluated in 114 patients suffering from Icenko- Cushing's syndrome .
Lymphocytic levels of glucocorticoid receptors were evaluated in 114 patients suffering from Icenko- proteinCushing's syndrome .
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1.5565 10.7971 1.0000 Incidence of proteinHLA antigens was determined in 94 of them.
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0.8530 1.0000 1.0000 A significant rise of proteinA10 and B27 antigen incidence compared to that in normal subjects allows these antigens to be considered genetic markers of Icenko- Cushing's syndrome .
0.9448 1.0000 1.0000 A significant rise of A10 and proteinB27 antigen incidence compared to that in normal subjects allows these antigens to be considered genetic markers of Icenko- Cushing's syndrome .
0.9218 1.0000 1.0000 A significant rise of A10 and B27 antigen incidence compared to that in normal subjects allows these proteinantigens to be considered genetic markers of Icenko- Cushing's syndrome .
A significant rise of A10 and proteinB27 antigen incidence compared to that in normal subjects allows these antigens to be considered genetic markers of Icenko- Cushing's syndrome .
A significant rise of A10 and B27 antigen incidence compared to that in normal subjects allows these antigens to be considered genetic markers of Icenko- proteinCushing's syndrome .
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2.4613 20.7084 1.0000 The levels of proteinglucocorticoid receptors in lymphocytes of the patients are lower than in normal subjects both in the active stage of the disease and following bilateral total adrenalectomy .
1.8585 10.3694 1.0000 The levels of glucocorticoid receptors in cell_typelymphocytes of the patients are lower than in normal subjects both in the active stage of the disease and following bilateral total adrenalectomy .
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2.4364 20.2122 1.0000 The patients carrying proteinB27 antigen had lymphocytic receptor concentrations under the levels of such in patients free of the antigen carriage.
1.7399 10.4249 1.0000 The patients carrying B27 antigen had proteinlymphocytic receptor concentrations under the levels of such in patients free of the antigen carriage.
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2.1358 20.4257 0.9999 Antigen B27 seems to be a cause of lower levels of proteinglucocorticoid receptors in blood lymphocytes .
1.4626 10.9658 0.9997 Antigen B27 seems to be a cause of lower levels of glucocorticoid receptors in cell_typeblood lymphocytes .
0.8584 0.9997 1.0000 proteinAntigen B27 seems to be a cause of lower levels of glucocorticoid receptors in blood lymphocytes .
0.9098 1.0000 1.0000 Antigen proteinB27 seems to be a cause of lower levels of glucocorticoid receptors in blood lymphocytes .
Antigen B27 seems to be a cause of lower levels of glucocorticoid receptors in blood cell_typelymphocytes .
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7.8007 30.8358 20.9915 Effects of 1 alpha, 25-dihydroxyvitamin D3 on the cell_linehuman chronic myelogenous leukemia cell line RWLeu-4 .
0.9102 0.9985 0.9993 Effects of 1 alpha, 25-dihydroxyvitamin D3 on the human chronic myelogenous leukemia cell line cell_lineRWLeu-4 .
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5.8081 40.5869 10.5465 The effects of 1 alpha, 25-dihydroxyvitamin D3 ( VD3 ) on proliferation , differentiation , and macromolecular synthesis in the new cell_linePhiladelphia chromosome-positive chronic myelogenous leukemia cell line , RWLeu-4 , were investigated.
0.9112 0.9999 1.0000 The effects of 1 alpha, 25-dihydroxyvitamin D3 ( VD3 ) on proliferation , differentiation , and macromolecular synthesis in the new Philadelphia chromosome-positive chronic myelogenous leukemia cell line , cell_lineRWLeu-4 , were investigated.
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1.5879 10.6688 0.9999 Treatment of cell_lineRWLeu-4 cells with VD3 induced 24R-hydroxylase activity , a marker of vitamin D3 responsiveness in many tissues.
0.9593 1.0000 1.0000 Treatment of RWLeu-4 cells with VD3 induced protein24R-hydroxylase activity , a marker of vitamin D3 responsiveness in many tissues.
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2.6394 20.0043 1.0000 Exposure of cell_lineRWLeu-4 cells to VD3 also inhibited proliferation and DNA synthesis with a 50% effective dose of 3.5-10 nM within 72 h; in addition, protein and RNA synthesis were inhibited by VD3 treatment .
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3.0361 20.4045 10.6848 Exposure of RWLeu-4 cells to 5 nM VD3 for 72 h caused 50% of the cells to differentiate into cell_typemacrophage/monocyte type cells as judged by nitroblue tetrazolium staining and adherence to plastic.
2.4311 20.8105 0.9999 Exposure of cell_lineRWLeu-4 cells to 5 nM VD3 for 72 h caused 50% of the cells to differentiate into macrophage/monocyte type cells as judged by nitroblue tetrazolium staining and adherence to plastic.
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3.8477 30.2432 10.3347 Progressive expression of proteincell surface maturation-specific antigens of the monocyte/macrophage lineage was induced by treatment of RWLeu-4 cells with VD3 for 24 to 72 h at doses that inhibited cellular proliferation .
2.2745 20.7661 0.9999 Progressive expression of cell surface maturation-specific antigens of the monocyte/macrophage lineage was induced by treatment of cell_lineRWLeu-4 cells with VD3 for 24 to 72 h at doses that inhibited cellular proliferation .
2.1003 20.4168 0.9999 Progressive expression of cell surface maturation-specific antigens of the cell_typemonocyte/macrophage lineage was induced by treatment of RWLeu-4 cells with VD3 for 24 to 72 h at doses that inhibited cellular proliferation .
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2.5708 20.3925 1.0000 c-myc RNA , which is constitutively expressed in cell_lineRWLeu-4 cells , increased after 0.5 h of treatment with 50 nM VD3 and then rapidly decreased to barely detectable levels after 4 h of treatment.
0.9515 0.9996 1.0000 RNAc-myc RNA , which is constitutively expressed in RWLeu-4 cells , increased after 0.5 h of treatment with 50 nM VD3 and then rapidly decreased to barely detectable levels after 4 h of treatment.
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3.7393 20.5437 10.4045 Finally, the in vitro tyrosine kinase activity associated with the proteinp210bcr-abl oncogene product was decreased approximately 50% by VD3 treatment .
1.4955 10.9370 0.9996 Finally, the in vitro proteintyrosine kinase activity associated with the p210bcr-abl oncogene product was decreased approximately 50% by VD3 treatment .
Finally, the in vitro tyrosine kinase activity associated with the DNAp210bcr-abl oncogene product was decreased approximately 50% by VD3 treatment .
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2.3419 20.0552 1.0000 Because of the presence of a functional proteinreceptor-effector system for VD3 and multiple biological responses to the hormone, these cells provide a unique model system with which to probe the specific effects of VD3 on cell growth and differentiation in chronic myelogenous leukemia .
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3.8004 30.0329 10.6919 A new member of the leucine zipper class of proteins that binds to the DNAHLA DR alpha promoter .
2.3373 20.5182 10.2914 A new member of the proteinleucine zipper class of proteins that binds to the HLA DR alpha promoter .
A new member of the proteinleucine zipper class of proteins that binds to the HLA DR alpha promoter .
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5.8164 30.9145 20.6614 Several mutants derived from cell_linetransformed human B cell lines are defective in expressing major histocompatibility complex (MHC) class II genes .
5.2392 30.1913 20.8714 Several mutants derived from transformed human B cell lines are defective in expressing DNAmajor histocompatibility complex (MHC) class II genes .
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5.4167 30.6367 10.6858 The failure to express a class II gene in at least one such mutant line has been mapped to the DNAMHC class II X box , a conserved transcriptional element in the promoter region .
3.2962 30.1420 10.2113 The failure to express a class II gene in at least one such mutant line has been mapped to the MHC class II X box , a DNAconserved transcriptional element in the promoter region .
3.2487 30.4832 10.6026 The failure to express a DNAclass II gene in at least one such mutant line has been mapped to the MHC class II X box , a conserved transcriptional element in the promoter region .
1.9967 20.8303 0.9997 The failure to express a class II gene in at least one such mutant line has been mapped to the MHC class II X box , a conserved transcriptional element in the DNApromoter region .
1.9142 20.3058 0.9999 The failure to express a class II gene in at least one such cell_linemutant line has been mapped to the MHC class II X box , a conserved transcriptional element in the promoter region .
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5.1583 30.5229 10.6772 A complementary DNA encoding a DNA-binding protein ( human X box binding protein , hXBP-1 ) whose target is the DNAhuman DR alpha X box and the 3' flanking region has now been cloned.
3.9420 20.3181 10.9409 A complementary DNA encoding a DNA-binding protein ( proteinhuman X box binding protein , hXBP-1 ) whose target is the human DR alpha X box and the 3' flanking region has now been cloned.
3.9395 30.3460 10.7807 A complementary DNA encoding a DNA-binding protein ( human X box binding protein , hXBP-1 ) whose target is the human DR alpha X box and the DNA3' flanking region has now been cloned.
1.3940 10.6813 0.9999 A DNAcomplementary DNA encoding a DNA-binding protein ( human X box binding protein , hXBP-1 ) whose target is the human DR alpha X box and the 3' flanking region has now been cloned.
1.3274 10.8290 0.9999 A complementary DNA encoding a proteinDNA-binding protein ( human X box binding protein , hXBP-1 ) whose target is the human DR alpha X box and the 3' flanking region has now been cloned.
0.9674 1.0000 1.0000 A complementary DNA encoding a DNA-binding protein ( human X box binding protein , proteinhXBP-1 ) whose target is the human DR alpha X box and the 3' flanking region has now been cloned.
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2.9574 20.9463 10.7475 This complementary DNA encoded a protein with structural similarities to the proteinc-jun proto-oncogene product , and its target sequence was closely related to the palindromic target sequence of c-jun .
2.8389 20.8250 10.7318 This complementary DNA encoded a protein with structural similarities to the c-jun proto-oncogene product , and its target sequence was closely related to the DNApalindromic target sequence of c-jun .
1.5292 10.9391 1.0000 This DNAcomplementary DNA encoded a protein with structural similarities to the c-jun proto-oncogene product , and its target sequence was closely related to the palindromic target sequence of c-jun .
0.8826 0.9999 1.0000 This complementary DNA encoded a protein with structural similarities to the c-jun proto-oncogene product , and its target sequence was closely related to the palindromic target sequence of DNAc-jun .
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3.4255 20.2047 10.9077 Mutation of the DNAhXBP-1 DNA target sequence decreased DR alpha promoter activity in vivo.
1.4608 10.8634 0.9989 Mutation of the hXBP-1 DNA target sequence decreased DNADR alpha promoter activity in vivo.
1.2490 10.4986 0.9977 Mutation of the proteinhXBP-1 DNA target sequence decreased DR alpha promoter activity in vivo.
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1.9111 20.1961 1.0000 These studies suggest that the proteinhXBP-1 protein acts as a transcription factor in B cells .
1.8741 20.3503 0.9902 These studies suggest that the proteinhXBP-1 protein acts as a transcription factor in B cells .
1.4723 10.8276 0.9996 These studies suggest that the hXBP-1 protein acts as a transcription factor in cell_typeB cells .
1.3699 10.9898 0.9999 These studies suggest that the hXBP-1 protein acts as a proteintranscription factor in B cells .
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3.6447 20.7117 10.1616 Absent or greatly diminished type I aldosterone receptors in cell_typeperipheral mononuclear leucocytes have been recently demonstrated and explain the lack of response to mineralocorticoids .
3.8374 20.7797 10.3985 Absent or greatly diminished proteintype I aldosterone receptors in peripheral mononuclear leucocytes have been recently demonstrated and explain the lack of response to mineralocorticoids .
Absent or greatly diminished type proteinI aldosterone receptors in peripheral mononuclear leucocytes have been recently demonstrated and explain the lack of response to mineralocorticoids .
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1.7837 10.8358 1.0000 In three families the autosomal recessive form was characterized by proteinnormal receptor as well as hormone data in both parents, while in one family receptor levels in both parents were greatly reduced, but hormone levels were normal.
0.9285 1.0000 1.0000 In three families the autosomal recessive form was characterized by normal receptor as well as hormone data in both parents, while in one family proteinreceptor levels in both parents were greatly reduced, but hormone levels were normal.
0.5145 1.0000 1.0000 In three families the autosomal recessive form was characterized by normal proteinreceptor as well as hormone data in both parents, while in one family receptor levels in both parents were greatly reduced, but hormone levels were normal.
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2.3633 30.4888 0.9999 In the four families with an autosomal dominant mode of transmission there was always one parent with reduced receptor binding in cell_typeperipheral mononuclear leucocytes and elevated serum hormone levels .
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3.6070 20.7131 10.5856 Perceived social support and tumor estrogen/progesterone receptor status as predictors of cell_typenatural killer cell activity in breast cancer patients .
0.7048 0.9998 1.0000 Perceived social support and tumor proteinestrogen/progesterone receptor status as predictors of natural killer cell activity in breast cancer patients .
2.0642 20.9890 10.6248 Perceived social support and proteintumor estrogen/progesterone receptor status as predictors of natural killer cell activity in breast cancer patients .
Perceived social support and tumor estrogen/progesterone receptor status as predictors of proteinnatural killer cell activity in breast cancer patients .
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5.8887 30.2105 10.4892 This report is concerned with the prediction of cell_typenatural killer (NK) cell activity in 61 Stage I and II breast cancer patients , between the ages of 25 and 70, who were accrued to this project.
This report is concerned with the prediction of natural cell_typekiller (NK) cell activity in 61 Stage I and II breast cancer patients , between the ages of 25 and 70, who were accrued to this project.
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1.8246 10.9271 1.0000 Higher NK activity could be predicted by the perception of high quality emotional support from a spouse or intimate other , perceived social support from the patient's physician , proteinestrogen receptor -negative tumor status , having an excisional biopsy as surgical treatment , and actively seeking social support as a major coping strategy (R2 = 0.33, F(5,55) = 5.5, p less than 0.0004).
Higher NK activity could be predicted by the perception of high quality emotional support from a spouse or intimate other , perceived social support from the patient's physician , estrogen receptor -negative tumor status , having an excisional biopsy as proteinsurgical treatment , and actively seeking social support as a major coping strategy (R2 = 0.33, F(5,55) = 5.5, p less than 0.0004).
Higher NK activity could be predicted by the perception of high quality emotional support from a spouse or intimate other , perceived social support from the patient's physician , estrogen receptor -negative tumor status , having an excisional biopsy as surgical treatment , and actively seeking proteinsocial support as a major coping strategy (R2 = 0.33, F(5,55) = 5.5, p less than 0.0004).
Higher NK activity could be predicted by the perception of high quality emotional support from a spouse or intimate other , perceived social support from the patient's physician , estrogen receptor -negative tumor status , having an proteinexcisional biopsy as surgical treatment , and actively seeking social support as a major coping strategy (R2 = 0.33, F(5,55) = 5.5, p less than 0.0004).
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Findings are discussed in terms of host interaction with proteintumor endocrine status , and the role that social support might play in modulating such activity.
Findings are discussed in terms of host interaction with tumor endocrine status , and the role that proteinsocial support might play in modulating such activity.
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2.8723 10.7748 10.3893 [ Estrogen receptor content of cell_typeperipheral blood lymphocytes in patients with systemic lupus erythematosus ]
1.5458 10.7142 1.0000 [ proteinEstrogen receptor content of peripheral blood lymphocytes in patients with systemic lupus erythematosus ]
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1.7965 10.2778 1.0000 ER content in cell_typelymphocytes of peripheral blood from 27 SLE patients and 20 healthy controls were determined by dextran-coated charcoal assay .
0.9859 1.0000 1.0000 proteinER content in lymphocytes of peripheral blood from 27 SLE patients and 20 healthy controls were determined by dextran-coated charcoal assay .
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3.6381 20.4459 10.5316 ER content in lymphocytes of each sample was expressed by both fmol/mg of proteinlymphocyte cytosolic protein and fmol/micrograms of lymphocyte DNA .
1.6227 10.8074 1.0000 ER content in cell_typelymphocytes of each sample was expressed by both fmol/mg of lymphocyte cytosolic protein and fmol/micrograms of lymphocyte DNA .
1.4638 10.6539 0.9998 ER content in lymphocytes of each sample was expressed by both fmol/mg of lymphocyte cytosolic protein and fmol/micrograms of DNAlymphocyte DNA .
0.9776 1.0000 1.0000 proteinER content in lymphocytes of each sample was expressed by both fmol/mg of lymphocyte cytosolic protein and fmol/micrograms of lymphocyte DNA .
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2.6517 20.1530 1.0000 The results showed that there was no significant difference between the proteinER content of lymphocytes from the controls and that from patients with SLE .
1.7928 10.7726 1.0000 The results showed that there was no significant difference between the ER content of cell_typelymphocytes from the controls and that from patients with SLE .
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2.5857 20.5183 1.0000 But the logarithmic mean of ER content in lymphocytes , expressed by fmol/mg of proteincytosolic protein , in 14 patients with active SLE (0.9356 +/- 0.31) was significantly higher than that in 13 patients with inactive SLE (0.2979 +/- 0.23, P less than 0.001) and in the controls (0.6204 +/- 0.52, P less than 0.001).
1.8614 10.8579 1.0000 But the logarithmic mean of ER content in cell_typelymphocytes , expressed by fmol/mg of cytosolic protein , in 14 patients with active SLE (0.9356 +/- 0.31) was significantly higher than that in 13 patients with inactive SLE (0.2979 +/- 0.23, P less than 0.001) and in the controls (0.6204 +/- 0.52, P less than 0.001).
1.8390 10.7491 1.0000 But the logarithmic mean of proteinER content in lymphocytes , expressed by fmol/mg of cytosolic protein , in 14 patients with active SLE (0.9356 +/- 0.31) was significantly higher than that in 13 patients with inactive SLE (0.2979 +/- 0.23, P less than 0.001) and in the controls (0.6204 +/- 0.52, P less than 0.001).
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1.8383 10.1509 1.0000 The normal upper limit of ER content in cell_typelymphocytes , expressed by fmol/micrograms of DNA, was 0.136.
1.7383 10.2370 1.0000 The normal upper limit of proteinER content in lymphocytes , expressed by fmol/micrograms of DNA, was 0.136.
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1.8342 10.8229 1.0000 The elevated rate of ER content in cell_typelymphocytes in 14 active SLE (92.9%) was also higher than that in quieiescent patients (23.1%, P less than 0.001) and in the controls (10%, P less than 0.001).
1.7835 10.7449 1.0000 The elevated rate of proteinER content in lymphocytes in 14 active SLE (92.9%) was also higher than that in quieiescent patients (23.1%, P less than 0.001) and in the controls (10%, P less than 0.001).
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2.3494 20.3415 0.9999 Moreover, the elevated level of ER content was found to be related to the positive proteinantidsDNA antibody and hypocomplementemia .
1.6600 10.7685 1.0000 Moreover, the elevated level of proteinER content was found to be related to the positive antidsDNA antibody and hypocomplementemia .
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3.7201 20.9381 10.8972 An in vitro globin gene switching model based on cell_typedifferentiated embryonic stem cells .
1.9679 20.3108 0.9998 An in vitro DNAglobin gene switching model based on differentiated embryonic stem cells .
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5.4728 20.4648 20.2980 We used cell_typemouse embryonic stem (ES) cells to study globin gene expression and switching in vitro.
1.8747 20.3019 0.9998 We used mouse embryonic stem (ES) cells to study DNAglobin gene expression and switching in vitro.
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4.7363 30.3907 10.9422 We show that ES-derived embryoid bodies express the full complement of DNAmouse embryonic globin genes in the correct temporal order and that on further differentiation , a switch occurs to the fetal/adult genes .
4.0520 20.6946 10.8983 We show that cell_typeES-derived embryoid bodies express the full complement of mouse embryonic globin genes in the correct temporal order and that on further differentiation , a switch occurs to the fetal/adult genes .
2.2336 20.5814 0.9999 We show that ES-derived embryoid bodies express the full complement of mouse embryonic globin genes in the correct temporal order and that on further differentiation , a switch occurs to the DNAfetal/adult genes .
0.5447 0.9989 0.9997 We show that ES-derived embryoid bodies express the full complement of mouse embryonic DNAglobin genes in the correct temporal order and that on further differentiation , a switch occurs to the fetal/adult genes .
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4.4089 30.0625 10.4075 In addition, the proteinerythroid-specific transcription factor NF-E1 was shown to be expressed coordinately with that of globin in embryoid bodies .
1.4741 10.9681 1.0000 In addition, the erythroid-specific transcription factor NF-E1 was shown to be expressed coordinately with that of proteinglobin in embryoid bodies .
0.9735 1.0000 1.0000 In addition, the erythroid-specific transcription factor proteinNF-E1 was shown to be expressed coordinately with that of globin in embryoid bodies .
In addition, the erythroid-specific transcription factor NF-E1 was shown to be expressed coordinately with that of globin in cell_typeembryoid bodies .
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2.3349 20.3637 10.2270 We conclude from these experiments that the cell_lineES cell system provides a good model to study hematopoietic development .
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3.7698 30.4188 10.3194 When the human epsilon- or beta- globin genes driven by the DNAdominant control region ( DCR ) are introduced into this system, the human epsilon- globin gene , in contrast to the beta- globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .
3.0086 30.6650 20.3970 When the human epsilon- or beta- globin genes driven by the dominant control region ( DCR ) are introduced into this system, the DNAhuman epsilon- globin gene , in contrast to the beta- globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .
2.9892 30.5356 10.5595 When the human epsilon- or beta- globin genes driven by the dominant control region ( DCR ) are introduced into this system, the human epsilon- globin gene , in contrast to the DNAbeta- globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .
2.2350 20.7607 0.9999 When the human epsilon- or beta- globin genes driven by the dominant control region ( DCR ) are introduced into this system, the human epsilon- globin gene , in contrast to the beta- globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an DNAembryonic gene .
0.9495 1.0000 1.0000 When the human epsilon- or beta- globin genes driven by the dominant control region ( DNADCR ) are introduced into this system, the human epsilon- globin gene , in contrast to the beta- globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .
0.8904 1.0000 1.0000 When the human epsilon- or beta- globin genes driven by the dominant control region ( DCR ) are introduced into this system, the human epsilon- globin gene , in contrast to the beta- globin gene , is not deregulated by the presence of the DNADCR and is expressed strictly as an embryonic gene .
When the human epsilon- or beta- globin genes driven by the dominant control region ( DCR ) are introduced into this system, the human epsilon- globin gene , in contrast to the beta- DNAglobin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .
When the human epsilon- or beta- globin genes driven by the dominant control region ( DCR ) are introduced into this system, the human epsilon- DNAglobin gene , in contrast to the beta- globin gene , is not deregulated by the presence of the DCR and is expressed strictly as an embryonic gene .
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3.7911 20.6331 10.4862 We conclude from this that the epsilon- globin gene is not regulated by competition with other genes in the DNAhuman beta-globin locus .
3.0531 20.5693 10.5414 We conclude from this that the DNAepsilon- globin gene is not regulated by competition with other genes in the human beta-globin locus .
We conclude from this that the epsilon- DNAglobin gene is not regulated by competition with other genes in the human beta-globin locus .
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4.4902 20.7409 10.7761 Cloning of a mitogen-inducible gene encoding a proteinkappa B DNA-binding protein with homology to the rel oncogene and to cell-cycle motifs .
1.9916 20.1966 0.9999 Cloning of a mitogen-inducible gene encoding a kappa B DNA-binding protein with homology to the DNArel oncogene and to cell-cycle motifs .
1.9766 20.4312 0.9996 Cloning of a mitogen-inducible gene encoding a kappa B DNA-binding protein with homology to the rel oncogene and to DNAcell-cycle motifs .
1.9338 20.7365 0.9999 Cloning of a DNAmitogen-inducible gene encoding a kappa B DNA-binding protein with homology to the rel oncogene and to cell-cycle motifs .
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3.6474 20.1377 10.7556 We have cloned and characterized a mitogen-inducible gene isolated from human T cells that predicts a protein of protein968 amino acids .
3.6463 20.0318 10.9442 We have cloned and characterized a mitogen-inducible gene isolated from cell_typehuman T cells that predicts a protein of 968 amino acids .
1.4404 10.9956 0.9999 We have cloned and characterized a DNAmitogen-inducible gene isolated from human T cells that predicts a protein of 968 amino acids .
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2.2763 20.3083 1.0000 The amino-terminal domain has regions homologous to the DNAoncogene rel and to the developmentally important gene dorsal of Drosophila .
1.6264 10.8025 1.0000 The proteinamino-terminal domain has regions homologous to the oncogene rel and to the developmentally important gene dorsal of Drosophila .
The amino-terminal domain has regions homologous to the oncogene rel and to the developmentally important gene DNAdorsal of Drosophila .
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2.3043 20.2728 0.9999 The carboxy-terminal domain contains repeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the putative human oncogene bcl-3 and in the proteinankyrin protein .
1.6464 10.5457 1.0000 The proteincarboxy-terminal domain contains repeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the putative human oncogene bcl-3 and in the ankyrin protein .
1.5423 10.0218 1.0000 The carboxy-terminal domain contains proteinrepeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the putative human oncogene bcl-3 and in the ankyrin protein .
0.5172 0.9996 0.9999 The carboxy-terminal domain contains repeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the putative human DNAoncogene bcl-3 and in the ankyrin protein .
The carboxy-terminal domain contains repeat structures found in a variety of proteins that are involved in cell-cycle control of yeast and in tissue differentiation in Drosophila and Ceanorhabditis elegans , as well as in the DNAputative human oncogene bcl-3 and in the ankyrin protein .
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4.0403 20.9422 10.4917 A truncated form of the product of this gene translated in vitro is a DNA-binding protein which interacts specifically with the DNAkappa B binding site found in many inducible genes , including the enhancer in human immunodeficiency virus .
2.3004 20.4693 1.0000 A truncated form of the product of this gene translated in vitro is a proteinDNA-binding protein which interacts specifically with the kappa B binding site found in many inducible genes , including the enhancer in human immunodeficiency virus .
2.2455 20.3328 1.0000 A truncated form of the product of this gene translated in vitro is a DNA-binding protein which interacts specifically with the kappa B binding site found in many DNAinducible genes , including the enhancer in human immunodeficiency virus .
1.7354 10.1981 1.0000 A truncated form of the product of this gene translated in vitro is a DNA-binding protein which interacts specifically with the kappa B binding site found in many inducible genes , including the DNAenhancer in human immunodeficiency virus .
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2.5712 20.0304 1.0000 This gene is yet another in a growing list of important proteinregulatory molecules whose expression is transcriptionally induced upon cellular activation .
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2.5235 20.0666 1.0000 Extrarenal receptor-effector-mechanisms for aldosterone : the sequence of effects on the cellular electrolyte transport in cell_typehuman lymphocytes and their implications for disorders of the water and electrolyte balances .
Extrarenal receptor-effector-mechanisms for aldosterone : the sequence of effects on the cellular electrolyte transport in human cell_typelymphocytes and their implications for disorders of the water and electrolyte balances .
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2.2286 20.9218 10.7186 High affinity aldosterone binding sites have not only been described in the classic target tissues such as the renal tubules , but also in non-classic target tissues such as the hippocampus , mammary gland , endothelial cells and, recently, cell_typehuman mononuclear leukocytes .
2.2124 20.5581 0.9991 High affinity aldosterone binding sites have not only been described in the classic target tissues such as the renal tubules , but also in non-classic target tissues such as the hippocampus , mammary gland , cell_typeendothelial cells and, recently, human mononuclear leukocytes .
1.7549 0.9970 10.3334 proteinHigh affinity aldosterone binding sites have not only been described in the classic target tissues such as the renal tubules , but also in non-classic target tissues such as the hippocampus , mammary gland , endothelial cells and, recently, human mononuclear leukocytes .
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3.8290 20.7020 10.4964 An in vitro effect of aldosterone on intracellular sodium , potassium and calcium concentrations and cell volume was shown in cell_typehuman mononuclear leukocytes .
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2.2848 20.6630 0.9999 The sodium/proton exchanger of the cell membrane could be identified as the primary target of the aldosterone action, possibly non-genomically mediated through proteinmembrane receptors .
1.6335 10.4762 1.0000 The proteinsodium/proton exchanger of the cell membrane could be identified as the primary target of the aldosterone action, possibly non-genomically mediated through membrane receptors .
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4.0342 20.7088 10.4872 The clinical significance of this model was underlined by the demonstration of absent or a decreased number of mineralocorticoid receptors and the lack of electrolyte response to aldosterone in cell_typehuman mononuclear leukocytes of patients with pseudohypoaldosteronism and aldosteronism .
2.4304 20.3921 1.0000 The clinical significance of this model was underlined by the demonstration of absent or a decreased number of proteinmineralocorticoid receptors and the lack of electrolyte response to aldosterone in human mononuclear leukocytes of patients with pseudohypoaldosteronism and aldosteronism .
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3.8183 20.2137 10.7555 Additionally, an abnormal effector mechanism could be demonstrated in cell_typehuman mononuclear leukocytes from essential hypertensives .
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4.7386 20.5401 10.4549 These studies are the first to demonstrate the significance of proteinextrarenal, nonepithelial mineralocorticoid receptors and the related effector mechanism in different disorders of the water and electrolyte balance in man .
0.7718 0.9988 0.9999 These studies are the first to demonstrate the significance of extrarenal, nonepithelial proteinmineralocorticoid receptors and the related effector mechanism in different disorders of the water and electrolyte balance in man .
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Immunohistochemical study of steroid hormones and an estrogen binding assay in cell_typemalignant soft tissue tumors .
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Immunohistochemically, the immunoreaction against 5 steroid hormone anti-sera ( estradiol , estriol , cortisol , progesterone and testosterone ) was examined in 39 cases with the cell_typemalignant soft tissue tumors ( fibrosarcoma : 8, malignant fibrous histiocytoma : 6, rhabdomyosarcoma : 10, leiomyosarcoma : 10, liposarcoma : 5).
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Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6899 0.9986 10.0991 Immunostained cell_typetumor cells were more frequently distributed in the area where tumor cell infiltration was more invasive.
cell_typeImmunostained tumor cells were more frequently distributed in the area where tumor cell infiltration was more invasive.
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Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6610 10.7190 1.0000 Furthermore, the existence of proteinestrogen receptor (estrogen binding activity) was examined histochemically in 39 cases and it was detected in 8.
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We concluded that steroid hormones might be closely related to tumor cell infiltration of some cell_typemalignant soft tissue tumors .
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4.3702 20.3993 10.8856 Involvement of proteincyclic AMP-dependent protein kinases in the signal transduction pathway for interleukin-1 .
1.3200 10.7008 1.0000 Involvement of cyclic AMP-dependent protein kinases in the signal transduction pathway for proteininterleukin-1 .
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6.0590 20.5170 20.7501 Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in interleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the DNAhuman immunodeficiency virus long terminal repeat .
3.5507 20.5854 10.9758 Expression of a highly specific protein inhibitor for proteincyclic AMP-dependent protein kinases in interleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat .
3.0220 20.9936 10.6467 Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in interleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the DNAkappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat .
2.1868 20.3177 0.9999 Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in cell_lineinterleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat .
0.8089 1.0000 0.9979 Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in proteininterleukin-1 (IL-1)-responsive cells blocked IL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat .
Expression of a highly specific protein inhibitor for cyclic AMP-dependent protein kinases in interleukin-1 (IL-1)-responsive cells blocked DNAIL-1-induced gene transcription that was driven by the kappa immunoglobulin enhancer or the human immunodeficiency virus long terminal repeat .
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4.5602 20.6355 10.8626 This inhibitor did not affect protein kinase C -mediated gene transcription , suggesting that proteincyclic AMP-dependent protein kinases are involved in the signal transduction pathway for IL-1 in a number of responsive cell types .
4.2736 20.8514 10.9321 This inhibitor did not affect protein kinase C -mediated gene transcription , suggesting that cyclic AMP-dependent protein kinases are involved in the signal transduction pathway for IL-1 in a number of cell_typeresponsive cell types .
4.0449 20.9608 10.8471 This inhibitor did not affect proteinprotein kinase C -mediated gene transcription , suggesting that cyclic AMP-dependent protein kinases are involved in the signal transduction pathway for IL-1 in a number of responsive cell types .
1.5421 10.3746 1.0000 This inhibitor did not affect protein kinase C -mediated gene transcription , suggesting that cyclic AMP-dependent protein kinases are involved in the signal transduction pathway for proteinIL-1 in a number of responsive cell types .
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1.5977 10.1787 0.9508 The DNAEpstein-Barr virus ( EBV ) ORI1yt enhancer is not B-cell specific and does not respond synergistically to the EBV transcription factors R and Z .
4.0267 30.6579 10.8672 The Epstein-Barr virus ( EBV ) ORI1yt enhancer is not B-cell specific and does not respond synergistically to the EBV proteintranscription factors R and Z .
1.7659 30.5398 10.1349 The Epstein-Barr virus ( EBV ) ORI1yt enhancer is not B-cell specific and does not respond synergistically to the proteinEBV transcription factors R and Z .
0.9229 1.0000 1.0000 The Epstein-Barr virus ( EBV ) ORI1yt enhancer is not B-cell specific and does not respond synergistically to the EBV transcription factors R and proteinZ .
0.7599 0.9994 1.0000 The Epstein-Barr virus ( EBV ) ORI1yt enhancer is not B-cell specific and does not respond synergistically to the EBV transcription factors proteinR and Z .
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3.2922 20.4208 10.9370 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the proteinBZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
2.0610 20.3362 1.0000 The Epstein-Barr virus DR promoter is located upstream of the DNAPstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
1.9933 20.2022 1.0000 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the DNATATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
1.5381 10.4676 0.9971 The DNAEpstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
1.5284 10.6442 1.0000 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to proteinEB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
1.4109 10.3212 0.9999 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an DNAupstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
0.9327 1.0000 1.0000 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and DNAB .
0.9094 1.0000 1.0000 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, DNAA and B .
0.8349 1.0000 1.0000 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 (Z) (the BZLF1-encoded transcription factor ) and an DNAenhancer with two functionally distinct domains, A and B .
2.3553 20.1594 0.9993 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to proteinEB1 (Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
0.6371 0.9999 1.0000 The Epstein-Barr virus DR promoter is located upstream of the PstI repeats , and in addition to the TATA box , it contains an upstream region (positions -69 to -220) responsive to EB1 protein(Z) (the BZLF1-encoded transcription factor ) and an enhancer with two functionally distinct domains, A and B .
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4.3925 30.0670 10.8975 Domain B has been described as a B-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and R , an EBV early product encoded by the DNAopen reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
3.5030 20.5771 10.1334 Domain B has been described as a B-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and R , an proteinEBV early product encoded by the open reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
2.3551 30.8872 10.3146 Domain B has been described as a DNAB-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and R , an EBV early product encoded by the open reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
0.9422 1.0000 1.0000 Domain B has been described as a B-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and proteinR , an EBV early product encoded by the open reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
0.8973 1.0000 1.0000 Domain B has been described as a B-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by proteinEB1 and R , an EBV early product encoded by the open reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
0.7964 0.9999 0.9999 Domain B has been described as a B-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and R , an EBV early product encoded by the open reading frame DNABRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
0.7446 0.9997 1.0000 DNADomain B has been described as a B-cell-specific EB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and R , an EBV early product encoded by the open reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
0.6374 1.0000 0.9955 Domain B has been described as a B-cell-specific proteinEB1 -responsive element (P.M.Lieberman, J.M.Hardwick, and S.D.Hayward, J.Virol.63:3040-3050, 1989) activated synergistically by EB1 and R , an EBV early product encoded by the open reading frame BRLF1 (M.A. Cox, J.Leahy, and J.M.Hardwick, J.Virol.64:313-321, 1990).
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3.2131 10.7424 10.6792 We show here that domain B is an R-responsive element in HeLa cells and is therefore not an DNAEB1 -responsive B-cell-specific element .
1.5673 10.1538 0.9999 We show here that domain B is an R-responsive element in cell_lineHeLa cells and is therefore not an EB1 -responsive B-cell-specific element .
1.4727 10.3592 1.0000 We show here that DNAdomain B is an R-responsive element in HeLa cells and is therefore not an EB1 -responsive B-cell-specific element .
1.3697 10.6242 1.0000 We show here that domain B is an DNAR-responsive element in HeLa cells and is therefore not an EB1 -responsive B-cell-specific element .
We show here that domain B is an R-responsive element in HeLa cells and is therefore not an proteinEB1 -responsive B-cell-specific element .
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3.5887 20.3879 10.5004 However, there is an EB1 -binding site ( ZRE-B ) located within the DNAR-responsive enhancer region .
3.5616 20.1462 10.8703 However, there is an DNAEB1 -binding site ( ZRE-B ) located within the R-responsive enhancer region .
0.9320 1.0000 1.0000 However, there is an EB1 -binding site ( DNAZRE-B ) located within the R-responsive enhancer region .
However, there is an proteinEB1 -binding site ( ZRE-B ) located within the R-responsive enhancer region .
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0.9619 1.0000 1.0000 DNAZRE-B can be deleted without affecting the R-dependent enhancer activity .
1.4102 10.9915 0.9999 ZRE-B can be deleted without affecting the DNAR-dependent enhancer activity .
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2.1776 20.4923 0.9999 Moreover, there is no cooperation or synergy between R and EB1 when activating the DNAB domain ( ZRE-B plus the R-responsive element ) positioned as an enhancer .
1.7369 10.5276 1.0000 Moreover, there is no cooperation or synergy between R and EB1 when activating the B domain ( DNAZRE-B plus the R-responsive element ) positioned as an enhancer .
1.5124 10.4122 1.0000 Moreover, there is no cooperation or synergy between R and EB1 when activating the B domain ( ZRE-B plus the DNAR-responsive element ) positioned as an enhancer .
0.8496 0.9999 1.0000 Moreover, there is no cooperation or synergy between proteinR and EB1 when activating the B domain ( ZRE-B plus the R-responsive element ) positioned as an enhancer .
0.8147 1.0000 1.0000 Moreover, there is no cooperation or synergy between R and EB1 when activating the B domain ( ZRE-B plus the R-responsive element ) positioned as an DNAenhancer .
0.8705 1.0000 1.0000 Moreover, there is no cooperation or synergy between R and DNAEB1 when activating the B domain ( ZRE-B plus the R-responsive element ) positioned as an enhancer .
Moreover, there is no cooperation or synergy between R and proteinEB1 when activating the B domain ( ZRE-B plus the R-responsive element ) positioned as an enhancer .
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2.8292 20.1258 10.6615 ZRE-B is therefore not part of the DNAR- inducible enhancer .
0.9541 1.0000 1.0000 DNAZRE-B is therefore not part of the R- inducible enhancer .
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4.1593 30.1449 10.6660 We have tested several subregions of the DR enhancer B domain , either alone or in combination, for their capacity to transmit the R-activating signal to the DNArabbit beta-globin promoter .
3.8949 20.8674 10.8059 We have tested several subregions of the DNADR enhancer B domain , either alone or in combination, for their capacity to transmit the R-activating signal to the rabbit beta-globin promoter .
We have tested several subregions of the DR enhancer DNAB domain , either alone or in combination, for their capacity to transmit the R-activating signal to the rabbit beta-globin promoter .
We have tested several subregions of the DNADR enhancer B domain , either alone or in combination, for their capacity to transmit the R-activating signal to the rabbit beta-globin promoter .
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2.2351 20.6110 1.0000 We found that the DNAR-responsive element is composed of four protoenhancers that span the whole B domain .
2.1819 20.4023 0.9999 We found that the R-responsive element is composed of four protoenhancers that span the whole DNAB domain .
1.6123 10.0269 1.0000 We found that the R-responsive element is composed of four DNAprotoenhancers that span the whole B domain .
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1.5550 10.4719 1.0000 These protoenhancers alone are weakly or not responsive to proteinR .
0.8577 0.9999 1.0000 These DNAprotoenhancers alone are weakly or not responsive to R .
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1.7138 10.1108 1.0000 One of the DNAprotoenhancers contains the overlapping palindromes 5'-TTGTCCcgtGGACAAaTGTCC-3' .
0.8877 0.9999 0.9996 One of the protoenhancers contains the overlapping DNApalindromes 5'-TTGTCCcgtGGACAAaTGTCC-3' .
0.6992 1.0000 0.9997 One of the protoenhancers contains the overlapping palindromes DNA5'-TTGTCCcgtGGACAAaTGTCC-3' .
0.5740 0.9998 0.9999 One of the protoenhancers contains the overlapping DNApalindromes 5'-TTGTCCcgtGGACAAaTGTCC-3' .
One of the protoenhancers contains the DNAoverlapping palindromes 5'-TTGTCCcgtGGACAAaTGTCC-3' .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7520 10.7565 1.0000 However, one DNApalindrome , either alone or duplicated, or the overlapping palindromes did not respond to R.
1.4496 10.8910 0.9999 However, one palindrome , either alone or duplicated, or the DNAoverlapping palindromes did not respond to R.
0.9267 1.0000 1.0000 However, one palindrome , either alone or duplicated, or the overlapping DNApalindromes did not respond to R.
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3.4407 20.5264 10.4013 Nuclear 3,5,3'-triiodothyronine receptors ( T3R ) of cell_typecirculating human lymphocytes in hyper- and hypo thyroidism and nonthyroidal diseases .
0.9662 1.0000 1.0000 Nuclear 3,5,3'-triiodothyronine receptors ( proteinT3R ) of circulating human lymphocytes in hyper- and hypo thyroidism and nonthyroidal diseases .
1.6107 0.9983 10.8193 proteinNuclear 3,5,3'-triiodothyronine receptors ( T3R ) of circulating human lymphocytes in hyper- and hypo thyroidism and nonthyroidal diseases .
Nuclear 3,5,3'-triiodothyronine receptors ( T3R ) of circulating human cell_typelymphocytes in hyper- and hypo thyroidism and nonthyroidal diseases .
Nuclear protein3,5,3'-triiodothyronine receptors ( T3R ) of circulating human lymphocytes in hyper- and hypo thyroidism and nonthyroidal diseases .
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1.7287 10.0761 1.0000 The clinical implications of nuclear proteinT3R alterations of circulating lymphocytes in hyperthyroidism , hypothyroidism and nonthyroidal diseases were investigated.
1.5718 10.8230 0.9999 The clinical implications of nuclear T3R alterations of cell_typecirculating lymphocytes in hyperthyroidism , hypothyroidism and nonthyroidal diseases were investigated.
The clinical implications of nuclear T3R alterations of circulating cell_typelymphocytes in hyperthyroidism , hypothyroidism and nonthyroidal diseases were investigated.
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1.7462 10.1396 1.0000 Nuclear T3R in cell_typelymphocytes was determined by radio-ligand binding analysis .
0.9476 1.0000 1.0000 Nuclear proteinT3R in lymphocytes was determined by radio-ligand binding analysis .
0.8773 0.9993 1.0000 proteinNuclear T3R in lymphocytes was determined by radio-ligand binding analysis .
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Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9146 20.8076 10.9795 In hyperthyroidism nuclear proteinT3 maximal binding capacity ( MBC ) was unaltered, whereas in hypothyroidism the MBC was significantly increased.
0.7395 1.0000 1.0000 In hyperthyroidism nuclear T3 maximal binding capacity ( proteinMBC ) was unaltered, whereas in hypothyroidism the MBC was significantly increased.
0.5593 1.0000 1.0000 In hyperthyroidism nuclear T3 maximal binding capacity ( MBC ) was unaltered, whereas in hypothyroidism the proteinMBC was significantly increased.
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1.8274 20.5239 0.9970 In the patients with diabetes mellitus , chronic renal failure and hepatic cirrhosis , the nuclear proteinT3R MBC of lymphocytes was about 1.5-1.6 times of the normal controls .
0.9123 0.9999 1.0000 In the patients with diabetes mellitus , chronic renal failure and hepatic cirrhosis , the nuclear T3R MBC of cell_typelymphocytes was about 1.5-1.6 times of the normal controls .
1.7797 20.5114 1.0000 In the patients with diabetes mellitus , chronic renal failure and hepatic cirrhosis , the nuclear proteinT3R MBC of lymphocytes was about 1.5-1.6 times of the normal controls .
0.9523 1.0000 1.0000 In the patients with diabetes mellitus , chronic renal failure and hepatic cirrhosis , the nuclear T3R proteinMBC of lymphocytes was about 1.5-1.6 times of the normal controls .
In the patients with diabetes mellitus , chronic renal failure and hepatic cirrhosis , the proteinnuclear T3R MBC of lymphocytes was about 1.5-1.6 times of the normal controls .
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2.5461 20.2886 1.0000 It was concluded that there existed hormonal regulation of proteinnuclear T3R , and up-regulation was seen in hypothyroidism and low T3 syndrome .
0.8581 1.0000 1.0000 It was concluded that there existed hormonal regulation of nuclear proteinT3R , and up-regulation was seen in hypothyroidism and low T3 syndrome .
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3.7107 20.9126 10.9035 Lymphocyte cell lines from vitamin D-dependent rickets type II show functional defects in the protein1 alpha,25-dihydroxyvitamin D3 receptor .
1.6008 0.9979 10.6985 cell_lineLymphocyte cell lines from vitamin D-dependent rickets type II show functional defects in the 1 alpha,25-dihydroxyvitamin D3 receptor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7123 0.9985 10.9294 cell_lineLymphocyte cell lines were established from five patients with vitamin D-dependent rickets , type II ( VDDR-II ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9155 20.7926 10.8132 Binding of [3H]1 alpha,25-dihydroxyvitamin D3 ( 1,25(OH)2D3 ) to its receptor in these cell lines was compared to binding studies using a cell_lineT-lymphocyte cell line ( S-LB1 ) from a normal individual.
0.9509 1.0000 1.0000 Binding of [3H]1 alpha,25-dihydroxyvitamin D3 ( 1,25(OH)2D3 ) to its receptor in these cell lines was compared to binding studies using a T-lymphocyte cell line ( cell_lineS-LB1 ) from a normal individual.
2.3495 20.1104 0.9999 Binding of [3H]1 alpha,25-dihydroxyvitamin D3 ( 1,25(OH)2D3 ) to its receptor in these cell_linecell lines was compared to binding studies using a T-lymphocyte cell line ( S-LB1 ) from a normal individual.
0.7854 0.9999 1.0000 Binding of [3H]1 alpha,25-dihydroxyvitamin D3 ( 1,25(OH)2D3 ) to its proteinreceptor in these cell lines was compared to binding studies using a T-lymphocyte cell line ( S-LB1 ) from a normal individual.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7754 20.8249 10.3817 The 1,25(OH)2D3 receptor of S-LB1 was comparable to the well-characterized proteinchick intestinal 1,25(OH)2D3 receptor in terms of its ligand binding affinity and capacity, its mobility on 5-20% sucrose gradients, and its adsorption to and elution properties from DNA-cellulose .
1.7971 10.1837 1.0000 The 1,25(OH)2D3 receptor of cell_lineS-LB1 was comparable to the well-characterized chick intestinal 1,25(OH)2D3 receptor in terms of its ligand binding affinity and capacity, its mobility on 5-20% sucrose gradients, and its adsorption to and elution properties from DNA-cellulose .
1.6591 10.6750 1.0000 The protein1,25(OH)2D3 receptor of S-LB1 was comparable to the well-characterized chick intestinal 1,25(OH)2D3 receptor in terms of its ligand binding affinity and capacity, its mobility on 5-20% sucrose gradients, and its adsorption to and elution properties from DNA-cellulose .
0.7729 0.9996 0.9999 The 1,25(OH)2D3 receptor of S-LB1 was comparable to the well-characterized chick intestinal protein1,25(OH)2D3 receptor in terms of its ligand binding affinity and capacity, its mobility on 5-20% sucrose gradients, and its adsorption to and elution properties from DNA-cellulose .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4813 20.8910 1.0000 Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cell_linecultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
1.6338 10.4993 0.9999 Three cell_linecell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
0.5864 0.9999 1.0000 Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a proteinreceptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
0.5632 1.0000 1.0000 Three cell lines established from patients with VDDR-II ( Rh- proteinVDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
2.4057 20.7576 0.9999 Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional protein1,25(OH)2D3 receptor .
2.3196 20.3042 1.0000 Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and proteinAb- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
1.7568 10.9971 1.0000 Three cell lines established from patients with VDDR-II ( Rh- VDR , proteinSh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
1.7148 10.8402 1.0000 Three cell lines established from patients with VDDR-II ( proteinRh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
1.5285 10.9687 0.9914 Three cell lines established from patients with VDDR-II ( Rh- VDR , proteinSh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
1.4225 10.8728 0.9876 Three cell lines established from patients with VDDR-II ( proteinRh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
1.0889 20.9562 0.9815 Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and proteinAb- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- proteinVDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and Ab- VDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a proteinfunctional 1,25(OH)2D3 receptor .
Three cell lines established from patients with VDDR-II ( Rh- VDR , Sh- VDR , and Ab- proteinVDR ) showed no specific binding of 1,25(OH)2D3 to a receptor and treatment of the cultured cells with 1,25(OH)2D3 did not stimulate production of 24,25-dihydroxy-vitamin D3 ( 24,25(OH)2D3 ), a response which is diagnostic of the presence of a functional 1,25(OH)2D3 receptor .
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1.5732 10.6519 0.9999 In a fourth cell_linecell line , A1-VDR , the receptor for 1,25(OH)2D3 had a low binding capacity and 25(OH)D3-24-hydroxylase activity was not detectable.
0.9399 1.0000 1.0000 In a fourth cell line , cell_lineA1-VDR , the receptor for 1,25(OH)2D3 had a low binding capacity and 25(OH)D3-24-hydroxylase activity was not detectable.
0.7807 1.0000 1.0000 In a fourth cell line , A1-VDR , the receptor for 1,25(OH)2D3 had a low binding capacity and protein25(OH)D3-24-hydroxylase activity was not detectable.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6874 30.2812 10.7218 Induction of 24,25-(OH)2D3 synthesis by 1,25(OH)2D3 was observed in the fifth cell line , designated Ro-VDR , although the sensitivity to hormone treatment was lower than in the cell_linecontrol cell line from a normal donor .
1.4464 10.5977 1.0000 Induction of 24,25-(OH)2D3 synthesis by 1,25(OH)2D3 was observed in the fifth cell line , designated cell_lineRo-VDR , although the sensitivity to hormone treatment was lower than in the control cell line from a normal donor .
3.8939 20.8749 10.9800 Induction of 24,25-(OH)2D3 synthesis by 1,25(OH)2D3 was observed in the cell_linefifth cell line , designated Ro-VDR , although the sensitivity to hormone treatment was lower than in the control cell line from a normal donor .
Induction of 24,25-(OH)2D3 synthesis by 1,25(OH)2D3 was observed in the fifth cell_linecell line , designated Ro-VDR , although the sensitivity to hormone treatment was lower than in the control cell line from a normal donor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6353 10.2684 1.0000 The capacity of the receptor for 1,25(OH)2D3 was low in cell_lineRo-VDR .
The capacity of the proteinreceptor for 1,25(OH)2D3 was low in Ro-VDR .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4505 20.5259 1.0000 In all cell_linecell lines where 1,25(OH)2D3 binding to a receptor was detectable, the receptor had the typical sedimentation coefficient of 3.7 S on sucrose density gradient analysis .
0.8971 1.0000 1.0000 In all cell lines where 1,25(OH)2D3 binding to a receptor was detectable, the proteinreceptor had the typical sedimentation coefficient of 3.7 S on sucrose density gradient analysis .
0.8756 1.0000 1.0000 In all cell lines where 1,25(OH)2D3 binding to a proteinreceptor was detectable, the receptor had the typical sedimentation coefficient of 3.7 S on sucrose density gradient analysis .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3718 20.3058 1.0000 Binding and elution properties to DNA-cellulose , however, differed from normal in both Ro-VDR and A1-VDR cells where elution from DNA-cellulose occurred at a lower salt concentration than is typical of the protein1,25(OH)2D3 receptor .
1.5896 10.8195 0.9999 Binding and elution properties to DNA-cellulose , however, differed from normal in both Ro-VDR and cell_lineA1-VDR cells where elution from DNA-cellulose occurred at a lower salt concentration than is typical of the 1,25(OH)2D3 receptor .
1.6960 10.1872 1.0000 Binding and elution properties to DNA-cellulose , however, differed from normal in both proteinRo-VDR and A1-VDR cells where elution from DNA-cellulose occurred at a lower salt concentration than is typical of the 1,25(OH)2D3 receptor .
Binding and elution properties to DNA-cellulose , however, differed from normal in both Ro-VDR and cell_lineA1-VDR cells where elution from DNA-cellulose occurred at a lower salt concentration than is typical of the 1,25(OH)2D3 receptor .
Binding and elution properties to DNA-cellulose , however, differed from normal in both Ro-VDR and A1-VDR cells where elution from DNA-cellulose occurred at a lower salt concentration than is typical of the 1,25(OH)2D3 proteinreceptor .
Binding and elution properties to DNA-cellulose , however, differed from normal in both cell_lineRo-VDR and A1-VDR cells where elution from DNA-cellulose occurred at a lower salt concentration than is typical of the 1,25(OH)2D3 receptor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7778 20.9432 10.8589 While Ro-VDR cells showed typical nuclear localization of the proteinunoccupied 1,25(OH)2D3 receptor , neither the unoccupied nor the occupied receptor from A1-VDR cells was completely localized in the nucleus .
2.4231 20.1327 1.0000 While Ro-VDR cells showed typical nuclear localization of the unoccupied 1,25(OH)2D3 receptor , neither the unoccupied nor the occupied receptor from cell_lineA1-VDR cells was completely localized in the nucleus .
1.6165 10.8645 0.9999 While cell_lineRo-VDR cells showed typical nuclear localization of the unoccupied 1,25(OH)2D3 receptor , neither the unoccupied nor the occupied receptor from A1-VDR cells was completely localized in the nucleus .
0.5635 1.0000 0.9999 While Ro-VDR cells showed typical nuclear localization of the unoccupied protein1,25(OH)2D3 receptor , neither the unoccupied nor the occupied receptor from A1-VDR cells was completely localized in the nucleus .
While Ro-VDR cells showed typical nuclear localization of the unoccupied 1,25(OH)2D3 receptor , neither the unoccupied nor the occupied proteinreceptor from A1-VDR cells was completely localized in the nucleus .
While Ro-VDR cells showed typical nuclear localization of the unoccupied 1,25(OH)2D3 proteinreceptor , neither the unoccupied nor the occupied receptor from A1-VDR cells was completely localized in the nucleus .
While Ro-VDR cells showed typical nuclear localization of the unoccupied 1,25(OH)2D3 receptor , neither the unoccupied nor the occupied receptor from cell_lineA1-VDR cells was completely localized in the nucleus .
While cell_lineRo-VDR cells showed typical nuclear localization of the unoccupied 1,25(OH)2D3 receptor , neither the unoccupied nor the occupied receptor from A1-VDR cells was completely localized in the nucleus .
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2.4700 20.0821 1.0000 In a series of functional studies we found that modulation of the level of the mRNAs coding for both the c-myc oncogene and the growth factor known as granulocyte-monocyte colony stimulating activity by 1,25(OH)2D3 correlated with the protein1,25(OH)2D3 receptor status of these cells.
2.3719 20.1537 1.0000 In a series of functional studies we found that modulation of the level of the mRNAs coding for both the DNAc-myc oncogene and the growth factor known as granulocyte-monocyte colony stimulating activity by 1,25(OH)2D3 correlated with the 1,25(OH)2D3 receptor status of these cells.
1.8190 10.4694 1.0000 In a series of functional studies we found that modulation of the level of the RNAmRNAs coding for both the c-myc oncogene and the growth factor known as granulocyte-monocyte colony stimulating activity by 1,25(OH)2D3 correlated with the 1,25(OH)2D3 receptor status of these cells.
1.6003 10.5839 0.9999 In a series of functional studies we found that modulation of the level of the mRNAs coding for both the c-myc oncogene and the proteingrowth factor known as granulocyte-monocyte colony stimulating activity by 1,25(OH)2D3 correlated with the 1,25(OH)2D3 receptor status of these cells.
In a series of functional studies we found that modulation of the level of the mRNAs coding for both the c-myc oncogene and the growth factor known as granulocyte-monocyte colony stimulating activity by 1,25(OH)2D3 correlated with the 1,25(OH)2D3 proteinreceptor status of these cells.
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2.5423 20.3376 0.9999 Use of these cell_linecell lines will facilitate further study of the molecular defect(s) in the receptor for 1,25(OH)2D3 in vitamin D-dependent rickets type II and will allow a correlation with impairment of cellular functions .
Use of these cell lines will facilitate further study of the molecular defect(s) in the proteinreceptor for 1,25(OH)2D3 in vitamin D-dependent rickets type II and will allow a correlation with impairment of cellular functions .
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1.4856 10.7858 1.0000 Transcriptional and post-transcriptional regulation of DNAc-jun expression during monocytic differentiation of human myeloid leukemic cells .
3.8686 20.7595 10.5729 Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of cell_typehuman myeloid leukemic cells .
Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of cell_linehuman myeloid leukemic cells .
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3.4954 20.2741 10.8651 AP-1 , the polypeptide product of c-jun , recognizes and binds to DNAspecific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate ( TPA ).
1.7232 10.1645 1.0000 AP-1 , the polypeptide product of DNAc-jun , recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate ( TPA ).
0.9827 1.0000 1.0000 proteinAP-1 , the polypeptide product of c-jun , recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate ( TPA ).
0.8924 1.0000 1.0000 AP-1 , the polypeptide product of c-jun , recognizes and binds to specific DNA sequences and stimulates transcription of DNAgenes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate ( TPA ).
1.6182 10.8834 1.0000 AP-1 , the polypeptide product of c-jun , recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain proteingrowth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate ( TPA ).
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2.0013 20.1748 0.9697 We studied the effects of TPA on the regulation of DNAc-jun gene expression in HL-60 cells during monocytic differentiation .
1.6220 10.9048 0.9999 We studied the effects of TPA on the regulation of c-jun gene expression in cell_lineHL-60 cells during monocytic differentiation .
2.1935 20.2897 1.0000 We studied the effects of TPA on the regulation of DNAc-jun gene expression in HL-60 cells during monocytic differentiation .
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3.9843 20.8176 10.6739 Low levels of c-jun transcripts were detectable in untreated cell_lineHL-60 leukemic cells , increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA .
1.9992 20.9663 1.0000 Low levels of proteinc-jun transcripts were detectable in untreated HL-60 leukemic cells , increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA .
Low levels of DNAc-jun transcripts were detectable in untreated HL-60 leukemic cells , increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA .
Low levels of c-jun transcripts were detectable in cell_lineuntreated HL-60 leukemic cells , increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA .
Low levels of RNAc-jun transcripts were detectable in untreated HL-60 leukemic cells , increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA .
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3.1955 10.7075 10.9019 Similar kinetics of c-jun induction by TPA were observed in human U-937 and cell_lineTHP-1 monocytic leukemia cells .
1.4431 10.8828 0.9996 Similar kinetics of c-jun induction by TPA were observed in cell_linehuman U-937 and THP-1 monocytic leukemia cells .
1.3537 10.9266 1.0000 Similar kinetics of DNAc-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells .
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3.9125 20.8879 10.2467 Similar findings were obtained with bryostatin 1 (10 nM), another activator of proteinprotein kinase C and inducer of monocytic differentiation .
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1.7703 10.1731 1.0000 Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation , increased DNAc-jun expression .
0.9223 0.9999 1.0000 Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces cell_lineHL-60 monocytic differentiation , increased c-jun expression .
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2.2837 20.3951 0.9999 TPA treatment of cell_lineHL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts.
1.8691 20.9699 0.9995 TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of DNAc-jun transcripts.
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1.6337 10.7214 0.9999 Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated cell_lineHL-60 cells , and that exposure to TPA increases this rate 3.3-fold.
2.3857 20.4051 1.0000 Run-on analysis demonstrated detectable levels of DNAc-jun gene transcription in untreated HL-60 cells , and that exposure to TPA increases this rate 3.3-fold.
Run-on analysis demonstrated detectable levels of DNAc-jun gene transcription in untreated HL-60 cells , and that exposure to TPA increases this rate 3.3-fold.
Run-on analysis demonstrated detectable levels of c-jun gene transcription in cell_lineuntreated HL-60 cells , and that exposure to TPA increases this rate 3.3-fold.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4182 20.1548 1.0000 Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of DNAc-jun transcription .
2.3698 20.2267 0.9999 Treatment of cell_lineHL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription .
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2.5101 20.6932 1.0000 The half-life of RNAc-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min.
1.5559 10.9301 0.9999 The half-life of c-jun RNA as determined by treating cell_lineHL-60 cells with TPA and actinomycin D was 30 min.
The half-life of DNAc-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min.
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3.0524 10.3048 10.5226 In contrast, the half-life of c-jun RNA in cell_lineTPA -treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h.
2.4656 20.4783 0.9999 In contrast, the half-life of RNAc-jun RNA in TPA -treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h.
0.8547 0.9984 0.9997 In contrast, the half-life of c-jun RNA in TPA -treated cell_lineHL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h.
In contrast, the half-life of DNAc-jun RNA in TPA -treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5851 20.7357 1.0000 These findings suggested that the increase in RNAc-jun RNA observed during TPA -induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms .
These findings suggested that the increase in DNAc-jun RNA observed during TPA -induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms .
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1.5427 10.9280 1.0000 [ Hormonal interactions and proteinglucocorticoid receptors in patients with the nephrotic syndrome ]
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
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2.5124 20.5044 1.0000 It is shown that the low level of steroid receptors , thyroid hormones that the low level of proteinsteroid receptors , thyroid hormones (T3 and T4) and cortisol is typical of children with the signs of renal dysplasia .
2.5054 20.6071 1.0000 It is shown that the low level of proteinsteroid receptors , thyroid hormones that the low level of steroid receptors , thyroid hormones (T3 and T4) and cortisol is typical of children with the signs of renal dysplasia .
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5.6504 30.4790 20.9096 Lymphoid specific gene expression of the DNAadenovirus early region 3 promoter is mediated by NF-kappa B binding motifs .
3.5726 20.9808 10.5224 Lymphoid specific gene expression of the adenovirus early region 3 promoter is mediated by DNANF-kappa B binding motifs .
1.6218 20.8422 0.9381 Lymphoid specific gene expression of the adenovirus early region 3 promoter is mediated by proteinNF-kappa B binding motifs .
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1.4906 10.8581 0.9997 A primary site of infection by human adenoviruses is cell_typelymphoid cells .
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3.5871 20.6652 10.3996 However, analysis of the DNAviral control elements and the cellular factors that regulate adenoviral gene expression in lymphocytes has not been reported.
1.6144 10.6544 1.0000 However, analysis of the viral control elements and the cellular factors that regulate adenoviral gene expression in cell_typelymphocytes has not been reported.
1.3958 10.9636 1.0000 However, analysis of the viral control elements and the proteincellular factors that regulate adenoviral gene expression in lymphocytes has not been reported.
1.4183 10.5120 0.9999 However, analysis of the viral control elements and the cellular factors that regulate DNAadenoviral gene expression in lymphocytes has not been reported.
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5.2868 30.7636 10.6365 The adenovirus early region 3 ( ES ) gene products are involved in the maintenance of viral persistence by complexing with the proteinclass I MHC antigens , thus preventing their cell surface expression with a resultant decrease in host immunologic destruction .
3.3734 10.7650 10.2707 The proteinadenovirus early region 3 ( ES ) gene products are involved in the maintenance of viral persistence by complexing with the class I MHC antigens , thus preventing their cell surface expression with a resultant decrease in host immunologic destruction .
The adenovirus early region 3 ( DNAES ) gene products are involved in the maintenance of viral persistence by complexing with the class I MHC antigens , thus preventing their cell surface expression with a resultant decrease in host immunologic destruction .
The DNAadenovirus early region 3 ( ES ) gene products are involved in the maintenance of viral persistence by complexing with the class I MHC antigens , thus preventing their cell surface expression with a resultant decrease in host immunologic destruction .
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2.4012 20.1006 0.9999 To determine whether different cellular factors were involved in E3 regulation in lymphocytes as compared with cell_lineHeLa cells , both DNA binding and transfection analysis with the E3 promoter in both cell types were performed.
2.2323 20.1505 1.0000 To determine whether different proteincellular factors were involved in E3 regulation in lymphocytes as compared with HeLa cells , both DNA binding and transfection analysis with the E3 promoter in both cell types were performed.
2.2029 20.3638 1.0000 To determine whether different cellular factors were involved in E3 regulation in lymphocytes as compared with HeLa cells , both DNA binding and transfection analysis with the DNAE3 promoter in both cell types were performed.
1.7173 10.3834 1.0000 To determine whether different cellular factors were involved in E3 regulation in cell_typelymphocytes as compared with HeLa cells , both DNA binding and transfection analysis with the E3 promoter in both cell types were performed.
1.9429 20.4587 0.9902 To determine whether different cellular factors were involved in E3 regulation in lymphocytes as compared with HeLa cells , both DNA binding and transfection analysis with the proteinE3 promoter in both cell types were performed.
0.8599 1.0000 1.0000 To determine whether different cellular factors were involved in proteinE3 regulation in lymphocytes as compared with HeLa cells , both DNA binding and transfection analysis with the E3 promoter in both cell types were performed.
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1.8273 10.3876 1.0000 These studies detected two novel domains referred to as DNAL1 and L2 with a variety of lymphoid but not HeLa extracts .
0.9546 1.0000 1.0000 These studies detected two novel domains referred to as L1 and DNAL2 with a variety of lymphoid but not HeLa extracts .
These studies detected two DNAnovel domains referred to as L1 and L2 with a variety of lymphoid but not HeLa extracts .
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0.9272 0.9997 0.9999 Each of these domains possessed strong homology to motifs previously found to bind the cellular factor proteinNF-kappa B .
1.3839 10.7423 0.9992 Each of these domains possessed strong homology to motifs previously found to bind the proteincellular factor NF-kappa B .
Each of these domains possessed strong homology to motifs previously found to bind the proteincellular factor NF-kappa B .
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4.8934 30.1838 10.5342 Transfections of E3 constructs linked to the chloramphenicol acetyltransferase gene revealed that mutagenesis of the DNAdistal NF-kappa B motif ( L2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
2.3095 20.7759 0.9999 Transfections of E3 constructs linked to the DNAchloramphenicol acetyltransferase gene revealed that mutagenesis of the distal NF-kappa B motif ( L2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
2.2052 20.6610 0.9999 Transfections of E3 constructs linked to the chloramphenicol acetyltransferase gene revealed that mutagenesis of the distal NF-kappa B motif ( L2 ) had minimal effects on promoter expression in cell_lineHeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
2.0507 20.9496 0.9997 Transfections of E3 constructs linked to the chloramphenicol acetyltransferase gene revealed that mutagenesis of the distal NF-kappa B motif ( L2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by cell_typelymphoid cells .
2.0315 20.3329 1.0000 Transfections of DNAE3 constructs linked to the chloramphenicol acetyltransferase gene revealed that mutagenesis of the distal NF-kappa B motif ( L2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
0.9470 1.0000 1.0000 Transfections of E3 constructs linked to the chloramphenicol acetyltransferase gene revealed that mutagenesis of the distal NF-kappa B motif ( DNAL2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
0.7555 1.0000 0.8949 Transfections of E3 constructs linked to the chloramphenicol acetyltransferase gene revealed that mutagenesis of the distal proteinNF-kappa B motif ( L2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
1.4534 20.9492 0.7368 Transfections of E3 constructs linked to the proteinchloramphenicol acetyltransferase gene revealed that mutagenesis of the distal NF-kappa B motif ( L2 ) had minimal effects on promoter expression in HeLa cells , but resulted in dramatic decreases in expression by lymphoid cells .
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4.9576 30.5387 10.9010 In contrast, mutagenesis of DNAproximal NF-kappa B motif ( L1 ) had minimal effects on gene expression in both HeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the L2 mutation .
2.2345 20.7527 0.9999 In contrast, mutagenesis of proximal NF-kappa B motif ( L1 ) had minimal effects on gene expression in both HeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in cell_typelymphoid cells when coupled to the L2 mutation .
2.2086 20.3573 0.9999 In contrast, mutagenesis of proximal NF-kappa B motif ( L1 ) had minimal effects on gene expression in both cell_lineHeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the L2 mutation .
1.6774 10.8105 0.9999 In contrast, mutagenesis of proximal NF-kappa B motif ( L1 ) had minimal effects on gene expression in both HeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the DNAL2 mutation .
1.4959 10.9932 0.9995 In contrast, mutagenesis of proximal NF-kappa B motif ( L1 ) had minimal effects on gene expression in both HeLa cells and cell_typelymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the L2 mutation .
0.9559 1.0000 1.0000 In contrast, mutagenesis of proximal NF-kappa B motif ( DNAL1 ) had minimal effects on gene expression in both HeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the L2 mutation .
1.6836 30.0081 0.8281 In contrast, mutagenesis of proximal proteinNF-kappa B motif ( L1 ) had minimal effects on gene expression in both HeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the L2 mutation .
0.4626 0.9996 0.9997 In contrast, mutagenesis of proximal DNANF-kappa B motif ( L1 ) had minimal effects on gene expression in both HeLa cells and lymphoid cells but resulted in a small, but reproducible, increase in gene expression in lymphoid cells when coupled to the L2 mutation .
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2.4776 20.3752 1.0000 Reversing the position and subsequent mutagenesis of the L1 and L2 domains indicated that the primary sequence of these motifs rather than their position in the DNAE3 promoter was critical for regulating gene expression .
2.3756 20.2712 1.0000 Reversing the position and subsequent mutagenesis of the L1 and L2 domains indicated that the DNAprimary sequence of these motifs rather than their position in the E3 promoter was critical for regulating gene expression .
0.7673 1.0000 1.0000 Reversing the position and subsequent mutagenesis of the DNAL1 and L2 domains indicated that the primary sequence of these motifs rather than their position in the E3 promoter was critical for regulating gene expression .
0.5641 0.9915 0.9999 Reversing the position and subsequent mutagenesis of the L1 and DNAL2 domains indicated that the primary sequence of these motifs rather than their position in the E3 promoter was critical for regulating gene expression .
0.5616 0.9998 0.9925 Reversing the position and subsequent mutagenesis of the L1 and DNAL2 domains indicated that the primary sequence of these motifs rather than their position in the E3 promoter was critical for regulating gene expression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5482 10.6346 1.0000 Characterization of proteindefensin resistance phenotypes associated with mutations in the phoP virulence regulon of Salmonella typhimurium .
3.6286 20.2889 10.3982 Characterization of defensin resistance phenotypes associated with mutations in the proteinphoP virulence regulon of Salmonella typhimurium .
Characterization of defensin resistance phenotypes associated with mutations in the DNAphoP virulence regulon of Salmonella typhimurium .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9490 20.3882 0.9995 The defensin sensitivities of Salmonella typhimurium strains with mutations in the phoP/phoQ two-component virulence regulon were tested by using proteinpurified defensins NP-1 and NP-2 .
0.9723 1.0000 1.0000 The defensin sensitivities of Salmonella typhimurium strains with mutations in the phoP/phoQ two-component virulence regulon were tested by using purified defensins proteinNP-1 and NP-2 .
0.9548 1.0000 1.0000 The defensin sensitivities of Salmonella typhimurium strains with mutations in the phoP/phoQ two-component virulence regulon were tested by using purified defensins NP-1 and proteinNP-2 .
0.8974 1.0000 1.0000 The proteindefensin sensitivities of Salmonella typhimurium strains with mutations in the phoP/phoQ two-component virulence regulon were tested by using purified defensins NP-1 and NP-2 .
4.0810 20.9410 10.9586 The defensin sensitivities of Salmonella typhimurium strains with mutations in the proteinphoP/phoQ two-component virulence regulon were tested by using purified defensins NP-1 and NP-2 .
0.6229 1.0000 0.9999 The defensin sensitivities of Salmonella typhimurium strains with mutations in the phoP/phoQ two-component virulence regulon were tested by using purified proteindefensins NP-1 and NP-2 .
The defensin sensitivities of Salmonella typhimurium strains with mutations in the DNAphoP/phoQ two-component virulence regulon were tested by using purified defensins NP-1 and NP-2 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0570 10.8875 10.6898 Strains with mutations in either gene of the regulatory pair ( phoP [ transcriptional activator ] or phoQ [ proteinmembrane sensor kinase ]) had increased sensitivities to defensin .
1.6680 10.7502 1.0000 Strains with mutations in either gene of the regulatory pair ( phoP [ transcriptional activator ] or DNAphoQ [ membrane sensor kinase ]) had increased sensitivities to defensin .
1.5186 10.2322 1.0000 Strains with mutations in either gene of the regulatory pair ( phoP [ transcriptional activator ] or phoQ [ membrane sensor kinase ]) had increased sensitivities to proteindefensin .
0.8928 0.9999 1.0000 Strains with mutations in either gene of the regulatory pair ( DNAphoP [ transcriptional activator ] or phoQ [ membrane sensor kinase ]) had increased sensitivities to defensin .
2.1422 20.2298 0.9999 Strains with mutations in either gene of the proteinregulatory pair ( phoP [ transcriptional activator ] or phoQ [ membrane sensor kinase ]) had increased sensitivities to defensin .
1.5188 10.4233 1.0000 Strains with mutations in either gene of the regulatory pair ( phoP [ proteintranscriptional activator ] or phoQ [ membrane sensor kinase ]) had increased sensitivities to defensin .
Strains with mutations in either gene of the DNAregulatory pair ( phoP [ transcriptional activator ] or phoQ [ membrane sensor kinase ]) had increased sensitivities to defensin .
Strains with mutations in either gene of the regulatory pair ( phoP [ DNAtranscriptional activator ] or phoQ [ membrane sensor kinase ]) had increased sensitivities to defensin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3115 20.2737 1.0000 The predicted proteinperiplasmic domain of the PhoQ protein contained a markedly anionic domain that could interact with cationic proteins and that could be responsible for resistance to defensin .
2.2824 20.0903 1.0000 The predicted periplasmic domain of the PhoQ protein contained a markedly anionic domain that could interact with proteincationic proteins and that could be responsible for resistance to defensin .
1.5132 10.7316 1.0000 The predicted periplasmic domain of the PhoQ protein contained a markedly anionic domain that could interact with cationic proteins and that could be responsible for resistance to proteindefensin .
1.4757 10.6776 1.0000 The predicted periplasmic domain of the proteinPhoQ protein contained a markedly anionic domain that could interact with cationic proteins and that could be responsible for resistance to defensin .
2.2930 20.0851 1.0000 The predicted periplasmic domain of the PhoQ protein contained a markedly proteinanionic domain that could interact with cationic proteins and that could be responsible for resistance to defensin .
1.8894 20.1537 0.9895 The predicted periplasmic domain of the proteinPhoQ protein contained a markedly anionic domain that could interact with cationic proteins and that could be responsible for resistance to defensin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1565 20.6239 10.1403 Because insertion mutations in phoP are polar on phoQ , we constructed strains that expressed the PhoQ protein in the absence of PhoP to test whether resistance to defensin requires only the proteinphoQ gene product .
2.2845 20.8326 1.0000 Because insertion mutations in phoP are polar on phoQ , we constructed strains that expressed the proteinPhoQ protein in the absence of PhoP to test whether resistance to defensin requires only the phoQ gene product .
1.6323 10.3327 1.0000 Because insertion mutations in phoP are polar on phoQ , we constructed strains that expressed the PhoQ protein in the absence of proteinPhoP to test whether resistance to defensin requires only the phoQ gene product .
1.3631 10.9243 1.0000 Because insertion mutations in DNAphoP are polar on phoQ , we constructed strains that expressed the PhoQ protein in the absence of PhoP to test whether resistance to defensin requires only the phoQ gene product .
1.2707 10.8600 1.0000 Because insertion mutations in phoP are polar on DNAphoQ , we constructed strains that expressed the PhoQ protein in the absence of PhoP to test whether resistance to defensin requires only the phoQ gene product .
1.8860 20.7841 0.9903 Because insertion mutations in phoP are polar on phoQ , we constructed strains that expressed the proteinPhoQ protein in the absence of PhoP to test whether resistance to defensin requires only the phoQ gene product .
1.6287 10.5481 1.0000 Because insertion mutations in phoP are polar on phoQ , we constructed strains that expressed the PhoQ protein in the absence of PhoP to test whether resistance to proteindefensin requires only the phoQ gene product .
Because insertion mutations in phoP are polar on phoQ , we constructed strains that expressed the PhoQ protein in the absence of PhoP to test whether resistance to defensin requires only the DNAphoQ gene product .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6955 10.5381 1.0000 We found that resistance to defensin requires the function of both components of this regulatory system , because strains expressing PhoQ without PhoP were still markedly sensitive to proteindefensins .
1.6453 10.8158 1.0000 We found that resistance to defensin requires the function of both components of this regulatory system , because strains expressing proteinPhoQ without PhoP were still markedly sensitive to defensins .
0.8764 1.0000 1.0000 We found that resistance to defensin requires the function of both components of this regulatory system , because strains expressing PhoQ without proteinPhoP were still markedly sensitive to defensins .
1.7480 10.6904 1.0000 We found that resistance to proteindefensin requires the function of both components of this regulatory system , because strains expressing PhoQ without PhoP were still markedly sensitive to defensins .
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.2847 30.5353 20.3600 This implied that a proteinpag ( phoP -activated gene ) product is responsible for defensin resistance .
1.4192 10.3296 1.0000 This implied that a pag ( phoP -activated gene ) product is responsible for proteindefensin resistance .
0.7255 1.0000 0.9946 This implied that a pag ( proteinphoP -activated gene ) product is responsible for defensin resistance .
This implied that a pag ( DNAphoP -activated gene ) product is responsible for defensin resistance .
This implied that a pag ( DNAphoP -activated gene ) product is responsible for defensin resistance .
This implied that a DNApag ( phoP -activated gene ) product is responsible for defensin resistance .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4808 10.6806 1.0000 We also tested for the ability of proteindefensins NP-1 , NP-5 , and HNP-1 to activate pag expression and found that these peptides have no effect.
0.9801 1.0000 1.0000 We also tested for the ability of defensins NP-1 , proteinNP-5 , and HNP-1 to activate pag expression and found that these peptides have no effect.
0.9554 1.0000 1.0000 We also tested for the ability of defensins proteinNP-1 , NP-5 , and HNP-1 to activate pag expression and found that these peptides have no effect.
0.9498 1.0000 1.0000 We also tested for the ability of defensins NP-1 , NP-5 , and proteinHNP-1 to activate pag expression and found that these peptides have no effect.
1.5842 10.4408 1.0000 We also tested for the ability of defensins NP-1 , NP-5 , and HNP-1 to activate proteinpag expression and found that these peptides have no effect.
We also tested for the ability of defensins NP-1 , NP-5 , and HNP-1 to activate DNApag expression and found that these peptides have no effect.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3980 20.4918 1.0000 Defensin resistance is not the only virulence characteristic controlled by the proteinPhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
2.3799 20.9217 1.0000 Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the DNAphoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
1.6955 10.5622 0.9999 Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within cell_typemacrophages .
0.9158 1.0000 1.0000 Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on proteindefensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
0.8834 1.0000 1.0000 Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype proteinPhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
1.6989 10.5819 1.0000 Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in proteinpagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
0.8768 1.0000 1.0000 Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive proteinpag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
0.4937 0.9996 0.9999 Defensin resistance is not the only virulence characteristic controlled by the PhoP protein-PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive DNApag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
Defensin resistance is not the only virulence characteristic controlled by the PhoP protein-PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in DNApagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
Defensin resistance is not the only virulence characteristic controlled by the proteinPhoP -PhoQ regulon because mutations in pagC , as well as ones in the phoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
Defensin resistance is not the only virulence characteristic controlled by the PhoP -PhoQ regulon because mutations in pagC , as well as ones in the DNAphoP locus that resulted in constitutive pag activation (phenotype PhoPc ), had no effect on defensin resistance , even though they rendered the organism avirulent and deficient in survival within macrophages .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7410 10.0696 1.0000 The virulence defect conferred by mutations in the phoP -phoQ two-component regulatory system is not completely explained by alterations in resistance to cationic proteins and involves the control of other proteins necessary for S. typhimurium survival within cell_typemacrophages .
1.5811 10.9391 1.0000 The virulence defect conferred by mutations in the phoP -phoQ two-component regulatory system is not completely explained by alterations in resistance to proteincationic proteins and involves the control of other proteins necessary for S. typhimurium survival within macrophages .
1.1744 10.1627 0.9973 The virulence defect conferred by mutations in the DNAphoP -phoQ two-component regulatory system is not completely explained by alterations in resistance to cationic proteins and involves the control of other proteins necessary for S. typhimurium survival within macrophages .
4.4758 30.2759 10.9456 The virulence defect conferred by mutations in the proteinphoP -phoQ two-component regulatory system is not completely explained by alterations in resistance to cationic proteins and involves the control of other proteins necessary for S. typhimurium survival within macrophages .
1.9572 20.1039 10.9083 The virulence defect conferred by mutations in the phoP protein-phoQ two-component regulatory system is not completely explained by alterations in resistance to cationic proteins and involves the control of other proteins necessary for S. typhimurium survival within macrophages .
The virulence defect conferred by mutations in the phoP DNA-phoQ two-component regulatory system is not completely explained by alterations in resistance to cationic proteins and involves the control of other proteins necessary for S. typhimurium survival within macrophages .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9637 20.9068 10.9591 Stimulation of a cell_linehuman T-cell clone with anti-CD3 or tumor necrosis factor induces NF-kappa B translocation but not human immunodeficiency virus 1 enhancer-dependent transcription .
2.6303 10.4652 10.6949 Stimulation of a human T-cell clone with anti-CD3 or proteintumor necrosis factor induces NF-kappa B translocation but not human immunodeficiency virus 1 enhancer-dependent transcription .
0.8418 0.9997 1.0000 Stimulation of a human T-cell clone with proteinanti-CD3 or tumor necrosis factor induces NF-kappa B translocation but not human immunodeficiency virus 1 enhancer-dependent transcription .
0.7587 0.9986 1.0000 Stimulation of a human T-cell clone with anti-CD3 or tumor necrosis factor induces proteinNF-kappa B translocation but not human immunodeficiency virus 1 enhancer-dependent transcription .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2656 20.9265 10.8541 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two human T-cell clones stimulated through their proteinT-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
3.6003 30.0411 10.6231 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two human T-cell clones stimulated through their T-cell receptor complex or by proteintumor necrosis factor or phorbol 12-myristate 13-acetate .
3.4866 20.8560 10.5946 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the proteinHIV enhancer-binding protein NF-kappa B were analyzed in two human T-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
3.4796 20.6603 10.8350 The expression of transiently transfected expression vectors under the control of the DNAlong terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two human T-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
2.1463 20.2344 0.9999 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its DNAenhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two human T-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
0.9560 1.0000 1.0000 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( DNALTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two human T-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
0.9112 0.9984 1.0000 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein proteinNF-kappa B were analyzed in two human T-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
3.6788 20.7233 10.9388 The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two cell_linehuman T-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
The expression of transiently transfected expression vectors under the control of the long terminal repeat ( LTR ) of the human immunodeficiency virus ( HIV ) or its enhancer sequence and the translocation of the HIV enhancer-binding protein NF-kappa B were analyzed in two human cell_lineT-cell clones stimulated through their T-cell receptor complex or by tumor necrosis factor or phorbol 12-myristate 13-acetate .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5406 10.5780 1.0000 We found a dissociation of proteinNF-kappa B translocation from transactivation of either the HIV LTR or the HIV enhancer .
1.5175 10.3955 0.9999 We found a dissociation of NF-kappa B translocation from transactivation of either the HIV LTR or the DNAHIV enhancer .
1.5089 10.5198 1.0000 We found a dissociation of NF-kappa B translocation from transactivation of either the DNAHIV LTR or the HIV enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4576 10.9262 1.0000 Interleukin 2 induced proliferation but not proteinNF-kappa B translocation or LTR transactivation .
0.9134 0.9999 1.0000 proteinInterleukin 2 induced proliferation but not NF-kappa B translocation or LTR transactivation .
0.7925 0.9999 1.0000 Interleukin 2 induced proliferation but not NF-kappa B translocation or DNALTR transactivation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6010 20.2610 10.7275 Phorbol ester or specific antigen recognition induced HIV LTR transactivation , whereas stimulation with proteintumor necrosis factor or antibody to CD3 did not.
1.4529 10.8344 0.9999 Phorbol ester or specific antigen recognition induced DNAHIV LTR transactivation , whereas stimulation with tumor necrosis factor or antibody to CD3 did not.
0.9855 1.0000 1.0000 Phorbol ester or specific antigen recognition induced HIV LTR transactivation , whereas stimulation with tumor necrosis factor or antibody to proteinCD3 did not.
1.6419 10.7340 10.0008 Phorbol ester or specific antigen recognition induced HIV LTR transactivation , whereas stimulation with tumor necrosis factor or proteinantibody to CD3 did not.
0.7930 1.0000 1.0000 Phorbol ester or specific antigen recognition induced HIV DNALTR transactivation , whereas stimulation with tumor necrosis factor or antibody to CD3 did not.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5064 20.5050 1.0000 The two latter signals were nevertheless able to induce proteinNF-kappa B translocation with a pattern in the band-shift assay indistinguishable from that observed using phorbol ester .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.0440 30.1346 10.9725 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from cell_typetumoral T cells in terms of requirements for HIV LTR activation .
4.4299 20.9954 10.8432 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cell_linecloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
3.6567 20.8865 10.9925 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most cell_linelymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
2.9554 10.6378 10.5100 Our finding that induction of NF-kappa B by proteintumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
2.1653 20.1577 1.0000 Our finding that induction of proteinNF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
2.1283 20.2914 1.0000 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for DNAHIV LTR activation .
1.4357 10.9559 0.9999 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce DNAHIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
1.2667 10.9500 0.9999 Our finding that induction of NF-kappa B by tumor necrosis factor or proteinantibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
4.1995 20.9276 10.7865 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that cell_typenormal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
0.9709 1.0000 1.0000 Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to proteinCD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal cell_typeT lymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
Our finding that induction of NF-kappa B by tumor necrosis factor or antibody to CD3 is not sufficient to induce HIV enhancer -dependent transcription in cloned T cells contrasts with results obtained in most lymphoblastoid T-cell lines and indicates that normal T cell_typelymphocytes differ from tumoral T cells in terms of requirements for HIV LTR activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0942 20.0089 0.9126 Furthermore, our results suggest that events linked to T-cell activation , in addition to NF-kappa B translocation per se, induce functional interactions of the proteinNF-kappa B complex with the HIV enhancer .
1.5254 10.4916 1.0000 Furthermore, our results suggest that events linked to T-cell activation , in addition to proteinNF-kappa B translocation per se, induce functional interactions of the NF-kappa B complex with the HIV enhancer .
1.4623 10.5361 0.9999 Furthermore, our results suggest that events linked to T-cell activation , in addition to NF-kappa B translocation per se, induce functional interactions of the NF-kappa B complex with the DNAHIV enhancer .
1.4433 10.7223 0.9999 Furthermore, our results suggest that events linked to T-cell activation , in addition to NF-kappa B translocation per se, induce functional interactions of the proteinNF-kappa B complex with the HIV enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6935 20.6253 10.6039 Decreased concentration of protein1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets : effect of phosphate supplementation .
3.0769 10.9986 10.4769 Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in cell_typeperipheral mononuclear cells of patients with X-linked hypophosphatemic rickets : effect of phosphate supplementation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6903 10.5303 1.0000 Since most of the actions of vitamin D are mediated by its receptors ( VDR ), abnormalities of proteinVDR have been postulated in XLH .
0.9437 1.0000 1.0000 Since most of the actions of vitamin D are mediated by its receptors ( proteinVDR ), abnormalities of VDR have been postulated in XLH .
1.6460 10.3432 1.0000 Since most of the actions of vitamin D are mediated by its proteinreceptors ( VDR ), abnormalities of VDR have been postulated in XLH .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1931 20.5250 10.6252 In order to investigate this possibility, we measured the concentration of VDR in cell_linePHA-activated peripheral mononuclear cells from 10 XLH patients .
1.4956 10.6842 1.0000 In order to investigate this possibility, we measured the concentration of proteinVDR in PHA-activated peripheral mononuclear cells from 10 XLH patients .
In order to investigate this possibility, we measured the concentration of VDR in PHA-activated cell_typeperipheral mononuclear cells from 10 XLH patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7488 10.4374 1.0000 There was a significant positive correlation between proteinVDR concentration and serum phosphate (P less than 0.05).
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7216 10.4442 1.0000 In two patients , proteinVDR was increased after daily phosphate supplementation was started.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6971 10.8517 1.0000 These results indicate that a decreased concentration of proteinVDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8572 20.5429 10.9127 Two distinct forms of active transcription factor CREB ( proteincAMP response element binding protein ).
1.7004 20.2061 0.9997 Two distinct forms of active proteintranscription factor CREB ( cAMP response element binding protein ).
0.6909 0.9955 0.9999 Two distinct forms of active transcription factor proteinCREB ( cAMP response element binding protein ).
Two distinct forms of proteinactive transcription factor CREB ( cAMP response element binding protein ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2032 20.5608 10.9254 Mammalian cells express two distinct forms of transcription factor CREB ( proteincAMP response element binding protein ) that are apparently the products of alternative splicing of the CREB gene transcript .
3.5488 20.9033 10.6467 Mammalian cells express two distinct forms of proteintranscription factor CREB ( cAMP response element binding protein ) that are apparently the products of alternative splicing of the CREB gene transcript .
3.1599 30.1419 0.9998 Mammalian cells express two distinct forms of transcription factor CREB ( cAMP response element binding protein ) that are apparently the products of alternative splicing of the RNACREB gene transcript .
0.8616 0.9997 0.9997 cell_typeMammalian cells express two distinct forms of transcription factor CREB ( cAMP response element binding protein ) that are apparently the products of alternative splicing of the CREB gene transcript .
0.7359 0.9995 1.0000 Mammalian cells express two distinct forms of transcription factor proteinCREB ( cAMP response element binding protein ) that are apparently the products of alternative splicing of the CREB gene transcript .
Mammalian cells express two distinct forms of transcription factor CREB ( cAMP response element binding protein ) that are apparently the products of alternative splicing of the proteinCREB gene transcript .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7710 20.4149 10.8740 The two proteins differ by a protein14-amino acid serine-rich insertion present in one of the CREB isoforms .
1.9053 20.0970 0.9999 The two proteins differ by a 14-amino acid serine-rich insertion present in one of the proteinCREB isoforms .
The two proteins differ by a 14-amino acid serine-rich insertion present in one of the proteinCREB isoforms .
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2.2317 20.5161 1.0000 We show that both proteinCREB isoforms are expressed in many cell types and mammalian species .
We show that both proteinCREB isoforms are expressed in many cell types and mammalian species .
We show that both CREB isoforms are expressed in cell_typemany cell types and mammalian species .
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3.7138 20.0858 10.6864 Both encode proteins that bind specifically to a DNAcAMP response element in vitro .
Both encode proteins that bind specifically to a DNAcAMP response element in vitro .
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1.5307 10.8817 1.0000 As expected for proteins of this class, the proteinCREB proteins bind DNA as dimers.
As expected for proteins of this class, the proteinCREB proteins bind DNA as dimers.
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1.4108 10.9811 1.0000 Both proteins impart cAMP -regulated transcriptional activity to a heterologous DNA-binding domain , showing that cAMP directly modulates the transcriptional stimulatory activity of proteinCREB .
3.7830 20.4653 10.4686 Both proteins impart cAMP -regulated transcriptional activity to a proteinheterologous DNA-binding domain , showing that cAMP directly modulates the transcriptional stimulatory activity of CREB .
Both proteins impart cAMP -regulated transcriptional activity to a DNAheterologous DNA-binding domain , showing that cAMP directly modulates the transcriptional stimulatory activity of CREB .
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2.9504 30.6419 0.9860 The presence of multiple proteinCREB isoforms with identical DNA-binding specificities but differences in the presumed regulatory domain raises the possibility that CREB proteins may be able to integrate distinct regulatory signals at the level of gene transcription .
2.3566 20.8673 1.0000 The presence of multiple CREB isoforms with identical DNA-binding specificities but differences in the presumed proteinregulatory domain raises the possibility that CREB proteins may be able to integrate distinct regulatory signals at the level of gene transcription .
2.1972 20.9684 1.0000 The presence of multiple proteinCREB isoforms with identical DNA-binding specificities but differences in the presumed regulatory domain raises the possibility that CREB proteins may be able to integrate distinct regulatory signals at the level of gene transcription .
2.1444 20.8999 1.0000 The presence of multiple CREB isoforms with identical DNA-binding specificities but differences in the presumed regulatory domain raises the possibility that proteinCREB proteins may be able to integrate distinct regulatory signals at the level of gene transcription .
1.4696 20.2525 0.9918 The presence of multiple CREB isoforms with identical DNA-binding specificities but differences in the presumed regulatory domain raises the possibility that proteinCREB proteins may be able to integrate distinct regulatory signals at the level of gene transcription .
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3.3993 30.4154 10.4269 Human immunodeficiency virus vpr product is a proteinvirion-associated regulatory protein .
1.6200 0.9969 10.5551 proteinHuman immunodeficiency virus vpr product is a virion-associated regulatory protein .
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2.3328 20.8785 0.9999 The vpr product of the human immunodeficiency virus type 1 ( HIV-1 ) acts in trans to accelerate virus replication and cytopathic effect in cell_typeT cells .
1.6922 10.7981 1.0000 The proteinvpr product of the human immunodeficiency virus type 1 ( HIV-1 ) acts in trans to accelerate virus replication and cytopathic effect in T cells .
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2.3056 20.5173 0.9999 Here it is shown that the HIV-1 viral particle contains multiple copies of the proteinvpr protein .
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1.6147 10.8430 1.0000 The proteinvpr product is the first regulatory protein of HIV-1 to be found in the virus particle .
2.3421 20.3279 1.0000 The vpr product is the first proteinregulatory protein of HIV-1 to be found in the virus particle .
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2.4524 20.1666 0.9999 This observation raises the possibility that vpr acts to facilitate the early steps of infection before de novo proteinviral protein synthesis occurs.
1.6851 10.8147 1.0000 This observation raises the possibility that proteinvpr acts to facilitate the early steps of infection before de novo viral protein synthesis occurs.
This observation raises the possibility that DNAvpr acts to facilitate the early steps of infection before de novo viral protein synthesis occurs.
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3.6838 20.9081 10.8954 A novel proteinB-cell lineage-specific transcription factor present at early but not late stages of differentiation .
0.8170 0.9934 0.9999 A novel B-cell lineage-specific proteintranscription factor present at early but not late stages of differentiation .
A novel B-cell lineage-specific transcription factor present at early but not late stages of proteindifferentiation .
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4.3429 20.9911 10.9224 A novel proteinB-cell-specific transcription factor , BSAP , was identified as a mammalian homolog of the sea urchin protein TSAP , which interacts with the promoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
3.5549 20.9496 10.5705 A novel B-cell-specific transcription factor , BSAP , was identified as a mammalian homolog of the proteinsea urchin protein TSAP , which interacts with the promoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
1.7241 10.1837 1.0000 A novel B-cell-specific transcription factor , BSAP , was identified as a mammalian homolog of the sea urchin protein TSAP , which interacts with the DNApromoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
0.9592 0.9999 1.0000 A novel B-cell-specific transcription factor , BSAP , was identified as a mammalian homolog of the sea urchin protein proteinTSAP , which interacts with the promoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
0.9527 1.0000 1.0000 A novel B-cell-specific transcription factor , proteinBSAP , was identified as a mammalian homolog of the sea urchin protein TSAP , which interacts with the promoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
0.7063 0.9996 0.9998 A novel B-cell-specific proteintranscription factor , BSAP , was identified as a mammalian homolog of the sea urchin protein TSAP , which interacts with the promoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
A novel B-cell-specific transcription factor , BSAP , was identified as a proteinmammalian homolog of the sea urchin protein TSAP , which interacts with the promoters of four tissue-specific late histone H2A-2 and H2B-2 genes .
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4.7530 20.9130 10.8272 As shown by mobility-shift , methylation interference , and mutational analyses , the mammalian protein BSAP recognizes all four DNAsea urchin binding sites in a manner indistinguishable from TSAP ; however, the two proteins differ in molecular weight.
1.6226 10.3552 1.0000 As shown by mobility-shift , methylation interference , and mutational analyses , the mammalian protein BSAP recognizes all four sea urchin binding sites in a manner indistinguishable from proteinTSAP ; however, the two proteins differ in molecular weight.
0.9544 1.0000 1.0000 As shown by mobility-shift , methylation interference , and mutational analyses , the mammalian protein proteinBSAP recognizes all four sea urchin binding sites in a manner indistinguishable from TSAP ; however, the two proteins differ in molecular weight.
4.5123 30.4194 10.7159 As shown by mobility-shift , methylation interference , and mutational analyses , the proteinmammalian protein BSAP recognizes all four sea urchin binding sites in a manner indistinguishable from TSAP ; however, the two proteins differ in molecular weight.
As shown by mobility-shift , methylation interference , and mutational analyses , the proteinmammalian protein BSAP recognizes all four sea urchin binding sites in a manner indistinguishable from TSAP ; however, the two proteins differ in molecular weight.
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0.9779 1.0000 1.0000 proteinBSAP is exclusively restricted to the B-cell lineage of lymphoid differentiation .
2.2310 20.2629 1.0000 BSAP is exclusively restricted to the cell_typeB-cell lineage of lymphoid differentiation .
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4.8259 30.1483 10.7868 Its expression appears to be activated during pro-B-cell development , is abundant at the pre-B- and mature B- cell stages , but is absent in cell_typeterminally differentiated plasma cells .
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4.2453 20.2826 10.6374 Moreover, BSAP is clearly a B-cell-specific transcription factor , as a wild-type but not a mutant TSAP -binding site of the sea urchin functions only in cell_linetransfected B cells as an upstream promoter element .
3.9716 20.9058 10.9053 Moreover, BSAP is clearly a B-cell-specific transcription factor , as a wild-type but not a mutant TSAP -binding site of the sea urchin functions only in transfected B cells as an DNAupstream promoter element .
3.7190 20.4122 10.6969 Moreover, BSAP is clearly a proteinB-cell-specific transcription factor , as a wild-type but not a mutant TSAP -binding site of the sea urchin functions only in transfected B cells as an upstream promoter element .
1.6160 10.1722 0.9972 Moreover, BSAP is clearly a B-cell-specific transcription factor , as a wild-type but not a mutant proteinTSAP -binding site of the sea urchin functions only in transfected B cells as an upstream promoter element .
0.8886 0.9999 1.0000 Moreover, proteinBSAP is clearly a B-cell-specific transcription factor , as a wild-type but not a mutant TSAP -binding site of the sea urchin functions only in transfected B cells as an upstream promoter element .
Moreover, BSAP is clearly a B-cell-specific transcription factor , as a DNAwild-type but not a mutant TSAP -binding site of the sea urchin functions only in transfected B cells as an upstream promoter element .
Moreover, BSAP is clearly a B-cell-specific transcription factor , as a wild-type but not a DNAmutant TSAP -binding site of the sea urchin functions only in transfected B cells as an upstream promoter element .
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3.3541 20.5676 10.9850 Competition experiments did not reveal any DNAhigh-affinity binding site for BSAP in known regulatory regions of immunoglobulin and class II major histocompatibility (MHC) genes , suggesting that BSAP is a regulator of a different set of B-lymphoid-specific genes .
2.0582 20.9000 0.9999 Competition experiments did not reveal any high-affinity binding site for BSAP in known regulatory regions of immunoglobulin and class II major histocompatibility (MHC) genes , suggesting that BSAP is a regulator of a different set of DNAB-lymphoid-specific genes .
1.2102 10.9355 0.9997 Competition experiments did not reveal any high-affinity binding site for BSAP in known DNAregulatory regions of immunoglobulin and class II major histocompatibility (MHC) genes , suggesting that BSAP is a regulator of a different set of B-lymphoid-specific genes .
0.8451 0.9999 1.0000 Competition experiments did not reveal any high-affinity binding site for proteinBSAP in known regulatory regions of immunoglobulin and class II major histocompatibility (MHC) genes , suggesting that BSAP is a regulator of a different set of B-lymphoid-specific genes .
0.8282 1.0000 1.0000 Competition experiments did not reveal any high-affinity binding site for BSAP in known regulatory regions of immunoglobulin and class II major histocompatibility (MHC) genes , suggesting that proteinBSAP is a regulator of a different set of B-lymphoid-specific genes .
5.3950 20.9153 20.9818 Competition experiments did not reveal any high-affinity binding site for BSAP in known regulatory regions of immunoglobulin and DNAclass II major histocompatibility (MHC) genes , suggesting that BSAP is a regulator of a different set of B-lymphoid-specific genes .
0.6780 0.9996 0.9997 Competition experiments did not reveal any high-affinity binding site for BSAP in known regulatory regions of proteinimmunoglobulin and class II major histocompatibility (MHC) genes , suggesting that BSAP is a regulator of a different set of B-lymphoid-specific genes .
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1.6539 0.9994 10.6069 proteinOctamer transcription factors and the cell type-specificity of immunoglobulin gene expression .
2.1516 20.1794 0.9999 Octamer transcription factors and the cell type-specificity of DNAimmunoglobulin gene expression .
Octamer transcription factors and the DNAcell type-specificity of immunoglobulin gene expression .
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1.2974 10.8038 0.9997 Antibodies are produced exclusively in cell_typeB lymphocytes .
0.9258 1.0000 1.0000 proteinAntibodies are produced exclusively in B lymphocytes .
Antibodies are produced exclusively in B cell_typelymphocytes .
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3.8693 20.6558 10.4993 The expression of the antibody-encoding genes , the DNAimmunoglobulin (Ig) genes , is also restricted to B cells .
2.0606 20.8335 0.9999 The expression of the DNAantibody-encoding genes , the immunoglobulin (Ig) genes , is also restricted to B cells .
1.9886 20.5712 0.9994 The expression of the antibody-encoding genes , the immunoglobulin (Ig) genes , is also restricted to cell_typeB cells .
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1.8106 10.0478 1.0000 The octamer sequence ATGCAAAT is present in the promoter and the DNAenhancer of Ig genes , and plays an important role in its tissue-specific expression .
1.6556 10.7139 1.0000 The octamer sequence ATGCAAAT is present in the promoter and the enhancer of DNAIg genes , and plays an important role in its tissue-specific expression .
1.5771 10.9477 0.9999 The DNAoctamer sequence ATGCAAAT is present in the promoter and the enhancer of Ig genes , and plays an important role in its tissue-specific expression .
0.9429 1.0000 1.0000 The octamer sequence ATGCAAAT is present in the DNApromoter and the enhancer of Ig genes , and plays an important role in its tissue-specific expression .
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3.6996 20.1232 10.9767 This sequence motif is a binding site for nuclear proteins , the so-called proteinoctamer transcription factors ( Oct or OTF factors ).
1.4472 10.4725 1.0000 This sequence motif is a binding site for proteinnuclear proteins , the so-called octamer transcription factors ( Oct or OTF factors ).
1.3767 10.4961 0.9998 This DNAsequence motif is a binding site for nuclear proteins , the so-called octamer transcription factors ( Oct or OTF factors ).
0.9382 1.0000 1.0000 This sequence motif is a binding site for nuclear proteins , the so-called octamer transcription factors ( proteinOct or OTF factors ).
0.7453 0.9987 1.0000 This sequence motif is a binding site for nuclear proteins , the so-called octamer transcription factors ( Oct or proteinOTF factors ).
1.3896 10.9306 0.9999 This sequence motif is a DNAbinding site for nuclear proteins , the so-called octamer transcription factors ( Oct or OTF factors ).
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2.1378 20.8276 0.9999 The Oct-1 protein is present in all cell types analyzed so far, whereas Oct-2A and Oct-2B are found mainly in cell_typeB lymphocytes .
1.4956 10.9105 1.0000 The proteinOct-1 protein is present in all cell types analyzed so far, whereas Oct-2A and Oct-2B are found mainly in B lymphocytes .
0.9587 1.0000 1.0000 The Oct-1 protein is present in all cell types analyzed so far, whereas Oct-2A and proteinOct-2B are found mainly in B lymphocytes .
0.9156 1.0000 1.0000 The Oct-1 protein is present in all cell types analyzed so far, whereas proteinOct-2A and Oct-2B are found mainly in B lymphocytes .
1.4610 10.8377 0.9878 The proteinOct-1 protein is present in all cell types analyzed so far, whereas Oct-2A and Oct-2B are found mainly in B lymphocytes .
The Oct-1 protein is present in all cell types analyzed so far, whereas Oct-2A and Oct-2B are found mainly in B cell_typelymphocytes .
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2.2916 10.2597 10.2248 It appears that the B cell-specific expression of Ig genes is mediated at least in part by cell type-specific Oct factors , and that there are both quantitative and qualitative differences between Oct-1 and proteinOct-2 factors .
2.1990 20.8345 0.9999 It appears that the B cell-specific expression of DNAIg genes is mediated at least in part by cell type-specific Oct factors , and that there are both quantitative and qualitative differences between Oct-1 and Oct-2 factors .
1.5801 10.1516 1.0000 It appears that the B cell-specific expression of Ig genes is mediated at least in part by cell type-specific Oct factors , and that there are both quantitative and qualitative differences between proteinOct-1 and Oct-2 factors .
3.9008 30.1660 10.5991 It appears that the B cell-specific expression of Ig genes is mediated at least in part by proteincell type-specific Oct factors , and that there are both quantitative and qualitative differences between Oct-1 and Oct-2 factors .
0.8235 0.9990 0.9999 It appears that the B cell-specific expression of Ig genes is mediated at least in part by cell type-specific proteinOct factors , and that there are both quantitative and qualitative differences between Oct-1 and Oct-2 factors .
It appears that the B cell-specific expression of Ig genes is mediated at least in part by cell proteintype-specific Oct factors , and that there are both quantitative and qualitative differences between Oct-1 and Oct-2 factors .
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2.9915 20.0924 10.1799 Recently, a number of other proteinoctamer factor variants were identified.
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1.6834 10.6249 1.0000 Many of these may be created by alternative splicing of a RNAprimary transcript of one Oct factor gene and may serve a specific function in the fine tuning of gene expression .
3.1531 20.3069 10.9732 Many of these may be created by alternative splicing of a primary transcript of one DNAOct factor gene and may serve a specific function in the fine tuning of gene expression .
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5.8969 30.2122 20.8528 A factor known to bind to DNAendogenous Ig heavy chain enhancer only in lymphocytes is a ubiquitously active transcription factor .
3.4486 20.4178 10.7324 A factor known to bind to endogenous Ig heavy chain enhancer only in lymphocytes is a proteinubiquitously active transcription factor .
1.4143 10.0908 1.0000 A factor known to bind to endogenous Ig heavy chain enhancer only in cell_typelymphocytes is a ubiquitously active transcription factor .
0.7200 0.9993 0.9998 A factor known to bind to endogenous Ig heavy chain enhancer only in lymphocytes is a ubiquitously active proteintranscription factor .
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5.2615 30.9422 10.6365 The transcriptional enhancer located in the first intron of the DNAimmunoglobulin heavy chain constant region is a major determinant of B-cell-specific expression of immunoglobulin genes .
1.8938 20.9554 0.9997 The transcriptional enhancer located in the first intron of the immunoglobulin heavy chain constant region is a major determinant of B-cell-specific expression of DNAimmunoglobulin genes .
1.3136 10.9559 0.9999 The DNAtranscriptional enhancer located in the first intron of the immunoglobulin heavy chain constant region is a major determinant of B-cell-specific expression of immunoglobulin genes .
1.8018 20.3911 0.9998 The transcriptional enhancer located in the DNAfirst intron of the immunoglobulin heavy chain constant region is a major determinant of B-cell-specific expression of immunoglobulin genes .
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4.4801 20.4115 10.8149 Like other enhancers , the DNAIg heavy chain enhancer contains several short sequence motifs that bind specific transcription factors .
1.6135 10.7953 1.0000 Like other DNAenhancers , the Ig heavy chain enhancer contains several short sequence motifs that bind specific transcription factors .
3.3614 20.3416 10.9489 Like other enhancers , the Ig heavy chain enhancer contains several DNAshort sequence motifs that bind specific transcription factors .
1.8921 20.5489 0.9998 Like other enhancers , the Ig heavy chain enhancer contains several short sequence motifs that bind specific proteintranscription factors .
Like other enhancers , the Ig heavy chain enhancer contains several short DNAsequence motifs that bind specific transcription factors .
Like other enhancers , the Ig heavy chain enhancer contains several short sequence motifs that bind proteinspecific transcription factors .
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1.7560 10.1868 1.0000 Each binding site contributes to the overall activity of the DNAenhancer , however no single element seems absolutely required for activity.
1.6424 10.4514 0.9999 Each DNAbinding site contributes to the overall activity of the enhancer , however no single element seems absolutely required for activity.
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3.9598 20.5102 10.9867 For a better understanding of the proteinIg heavy chain enhancer components , we have cloned and analyzed individual sequence elements .
3.3024 20.9331 10.7986 For a better understanding of the proteinIg heavy chain enhancer components , we have cloned and analyzed individual sequence elements .
1.2042 0.9947 10.2698 For a better understanding of the Ig heavy chain proteinenhancer components , we have cloned and analyzed individual sequence elements .
For a better understanding of the DNAIg heavy chain enhancer components , we have cloned and analyzed individual sequence elements .
For a better understanding of the DNAIg heavy chain enhancer components , we have cloned and analyzed individual sequence elements .
For a better understanding of the Ig heavy chain enhancer components , we have cloned and analyzed individual DNAsequence elements .
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3.5356 20.6474 10.5561 We find that the factor that binds to the DNAE3 enhancer motif , CATGTGGC , is a ubiquitous transcription factor .
3.4803 20.9780 10.7355 We find that the factor that binds to the E3 enhancer motif , CATGTGGC , is a proteinubiquitous transcription factor .
0.5795 0.9996 1.0000 We find that the factor that binds to the E3 enhancer motif , DNACATGTGGC , is a ubiquitous transcription factor .
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2.4932 10.8256 10.2265 It is present in an active form in both B cells and cell_typenon- B cells , where it can mediate transcriptional activation in vitro and in vivo.
2.3270 20.1308 0.9998 It is present in an active form in both cell_typeB cells and non- B cells , where it can mediate transcriptional activation in vitro and in vivo.
0.7947 1.0000 0.9998 It is present in an active form in both B cells and non- cell_typeB cells , where it can mediate transcriptional activation in vitro and in vivo.
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6.3501 30.3228 20.6447 However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the DNAendogenous Ig heavy chain enhancer in non- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in B cells but not in non-B cells .
3.2505 20.8151 10.9413 However, despite its ability to activate transcription of a DNAtransfected reporter gene , the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in non- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in B cells but not in non-B cells .
2.2864 20.5546 0.9999 However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in non- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in cell_typeB cells but not in non-B cells .
2.2842 10.6817 10.0723 However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in cell_typenon- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in B cells but not in non-B cells .
2.2787 20.2879 0.9997 However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in non- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in B cells but not in cell_typenon-B cells .
1.6599 10.9835 1.0000 However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in non- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated proteinNF-muE3 , was detected in B cells but not in non-B cells .
0.6967 1.0000 0.9997 However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the endogenous Ig heavy chain enhancer in non- cell_typelymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in B cells but not in non-B cells .
However, despite its ability to activate transcription of a transfected reporter gene , the factor is apparently unable to bind to the endogenous DNAIg heavy chain enhancer in non- lymphoid cells : In previous experiments by others, the characteristic in vivo footprint of this factor, designated NF-muE3 , was detected in B cells but not in non-B cells .
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4.8565 20.1165 10.6865 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) proteinubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
2.3406 20.0056 1.0000 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) proteincell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
2.2496 20.8818 0.9999 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in cell_typeB lymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
1.6711 10.7108 1.0000 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as proteinOct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
1.6245 10.5133 1.0000 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) proteinubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
1.5895 10.9316 0.9999 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in cell_typeB cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
1.5708 10.8743 1.0000 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as proteinNF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
1.4348 30.5308 0.9998 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the DNAE3 sequence motif .
0.9528 1.0000 1.0000 From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B lymphocytes : (a) cell-specific factors such as Oct-2A and proteinOct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
From this and other findings the picture emerges that there are at least three categories of factors which mediate cell-type-specific transcription in B cell_typelymphocytes : (a) cell-specific factors such as Oct-2A and Oct-2B that are not expressed in most other cell types: (b) ubiquitous factors such as NF-kappa B that are constitutively active in B cells but are sequestered in an inactive form in other cells; (c) ubiquitously active factors , exemplified by the one binding to the E3 sequence motif .
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4.6249 20.3245 10.9337 This factor is present in an active form in a variety of cell types but is apparently unable to bind to the DNAendogenous Ig heavy chain enhancer in non-B cells , perhaps due to a non-permissive chromatin structure of the Ig heavy chain locus .
3.7536 20.6185 10.9642 This factor is present in an active form in a variety of cell types but is apparently unable to bind to the endogenous Ig heavy chain enhancer in non-B cells , perhaps due to a non-permissive chromatin structure of the DNAIg heavy chain locus .
1.6193 10.1414 0.9999 This factor is present in an active form in a variety of cell types but is apparently unable to bind to the endogenous Ig heavy chain enhancer in cell_typenon-B cells , perhaps due to a non-permissive chromatin structure of the Ig heavy chain locus .
3.6341 20.2218 10.8002 This factor is present in an active form in a variety of cell types but is apparently unable to bind to the endogenous Ig heavy chain enhancer in non-B cells , perhaps due to a DNAnon-permissive chromatin structure of the Ig heavy chain locus .
This factor is present in an active form in a variety of cell types but is apparently unable to bind to the endogenous Ig heavy chain enhancer in non-B cells , perhaps due to a non-permissive DNAchromatin structure of the Ig heavy chain locus .
This factor is present in an active form in a variety of cell types but is apparently unable to bind to the endogenous DNAIg heavy chain enhancer in non-B cells , perhaps due to a non-permissive chromatin structure of the Ig heavy chain locus .
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2.6001 20.3797 1.0000 A study was made of adrenocortical function by measuring blood plasma cortisol concentration and amount of proteinglucocorticoid receptors in lymphocytes as well as thyroid function by measuring blood plasma triidothyronine and thyroxine concentration in 58 bronchial asthma children aged 1 to 14 years.
0.9476 1.0000 1.0000 A study was made of adrenocortical function by measuring blood plasma cortisol concentration and amount of glucocorticoid receptors in cell_typelymphocytes as well as thyroid function by measuring blood plasma triidothyronine and thyroxine concentration in 58 bronchial asthma children aged 1 to 14 years.
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1.4654 10.8940 0.9998 TAR independent activation of the human immunodeficiency virus in phorbol ester stimulated cell_typeT lymphocytes .
0.9190 1.0000 1.0000 DNATAR independent activation of the human immunodeficiency virus in phorbol ester stimulated T lymphocytes .
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8.0061 30.9362 20.7545 Multiple regulatory elements in the DNAhuman immunodeficiency virus long terminal repeat ( HIV LTR ) are required for activation of HIV gene expression .
1.4592 10.3337 0.9999 Multiple regulatory elements in the human immunodeficiency virus long terminal repeat ( DNAHIV LTR ) are required for activation of HIV gene expression .
1.2529 10.9314 0.9999 Multiple DNAregulatory elements in the human immunodeficiency virus long terminal repeat ( HIV LTR ) are required for activation of HIV gene expression .
1.2133 10.7667 0.9998 Multiple regulatory elements in the human immunodeficiency virus long terminal repeat ( HIV LTR ) are required for activation of DNAHIV gene expression .
Multiple regulatory elements in the human immunodeficiency virus DNAlong terminal repeat ( HIV LTR ) are required for activation of HIV gene expression .
DNAMultiple regulatory elements in the human immunodeficiency virus long terminal repeat ( HIV LTR ) are required for activation of HIV gene expression .
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3.7492 20.4298 10.6755 Previous transfection studies of HIV LTR constructs linked to the DNAchloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , SP1 , TATA and TAR regions were important for HIV gene expression .
2.9763 20.9761 10.5142 Previous transfection studies of DNAHIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , SP1 , TATA and TAR regions were important for HIV gene expression .
1.6412 10.2485 1.0000 Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the DNAenhancer , SP1 , TATA and TAR regions were important for HIV gene expression .
0.9051 1.0000 1.0000 Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , DNASP1 , TATA and TAR regions were important for HIV gene expression .
0.6496 1.0000 1.0000 Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , SP1 , DNATATA and TAR regions were important for HIV gene expression .
0.5667 0.9994 0.9998 Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple DNAregulatory regions including the enhancer , SP1 , TATA and TAR regions were important for HIV gene expression .
3.3287 20.7771 10.6952 Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that DNAmultiple regulatory regions including the enhancer , SP1 , TATA and TAR regions were important for HIV gene expression .
0.5589 1.0000 0.9993 Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , SP1 , TATA and DNATAR regions were important for HIV gene expression .
Previous transfection studies of DNAHIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , SP1 , TATA and TAR regions were important for HIV gene expression .
Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer , SP1 , TATA and DNATAR regions were important for HIV gene expression .
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2.0500 20.6490 0.9999 To characterize these DNAregulatory elements further, mutations in these regions were inserted into both the 5' and 3' HIV LTRs and infectious proviral constructs were assembled.
0.8029 0.9631 0.9984 To characterize these regulatory elements further, mutations in these regions were inserted into both the 5' and 3' DNAHIV LTRs and infectious proviral constructs were assembled.
4.5885 20.7231 10.9980 To characterize these regulatory elements further, mutations in these regions were inserted into both the DNA5' and 3' HIV LTRs and infectious proviral constructs were assembled.
2.1463 10.6970 10.5984 To characterize these regulatory elements further, mutations in these regions were inserted into both the 5' and 3' HIV LTRs and DNAinfectious proviral constructs were assembled.
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2.4785 20.4134 0.9999 These constructs were transfected into either cell_lineHeLa cells , Jurkat cells or U937 cells in both the presence and absence of phorbol esters which have previously been demonstrated to activate HIV gene expression .
1.7487 10.5625 0.9999 These constructs were transfected into either HeLa cells , cell_lineJurkat cells or U937 cells in both the presence and absence of phorbol esters which have previously been demonstrated to activate HIV gene expression .
1.7222 10.6673 0.9999 These constructs were transfected into either HeLa cells , Jurkat cells or cell_lineU937 cells in both the presence and absence of phorbol esters which have previously been demonstrated to activate HIV gene expression .
1.4186 10.7953 0.9998 These constructs were transfected into either HeLa cells , Jurkat cells or U937 cells in both the presence and absence of phorbol esters which have previously been demonstrated to activate DNAHIV gene expression .
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3.7190 20.9281 10.5128 Viral gene expression was assayed by the level of proteinp24 gag protein released from cultures transfected with the proviral constructs .
2.2009 20.4120 0.9999 Viral gene expression was assayed by the level of p24 gag protein released from cultures transfected with the DNAproviral constructs .
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2.9954 10.6521 10.5982 Results in all cell lines indicated that mutations of the SP1 , TATA and the TAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or DNATAR primary sequence resulted in only slight decreases.
2.7872 10.7281 10.7188 Results in all cell lines indicated that mutations of the SP1 , TATA and the TAR loop and DNAstem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or TAR primary sequence resulted in only slight decreases.
2.0525 20.1742 0.9998 Results in all cell lines indicated that mutations of the SP1 , TATA and the TAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the DNAenhancer motif or TAR primary sequence resulted in only slight decreases.
1.6331 10.0295 1.0000 Results in all cell lines indicated that mutations of the DNASP1 , TATA and the TAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or TAR primary sequence resulted in only slight decreases.
1.3592 10.9903 0.9999 Results in all cell lines indicated that mutations of the SP1 , TATA and the DNATAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or TAR primary sequence resulted in only slight decreases.
0.8904 1.0000 1.0000 Results in all cell lines indicated that mutations of the SP1 , DNATATA and the TAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or TAR primary sequence resulted in only slight decreases.
2.2587 20.6006 0.9999 Results in all cell_linecell lines indicated that mutations of the SP1 , TATA and the TAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or TAR primary sequence resulted in only slight decreases.
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6.4934 30.3211 10.9938 However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated Jurkat cells but not in cell_linephorbol ester -treated HeLa or U937 cells .
6.2266 30.3511 10.4778 However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in cell_linephorbol ester -treated Jurkat cells but not in phorbol ester -treated HeLa or U937 cells .
2.3844 20.2810 0.9999 However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated cell_lineJurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated Jurkat cells but not in phorbol ester -treated HeLa or U937 cells .
2.3487 20.7289 0.9997 However, viruses containing mutations in either the DNATAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated Jurkat cells but not in phorbol ester -treated HeLa or U937 cells .
2.2644 10.4970 10.1960 However, viruses containing mutations in either the TAR loop sequences or DNAstem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated Jurkat cells but not in phorbol ester -treated HeLa or U937 cells .
1.6043 10.2264 0.9995 However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated Jurkat cells but not in phorbol ester -treated HeLa or cell_lineU937 cells .
0.8454 0.9981 0.9998 However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated cell_lineJurkat cells but not in phorbol ester -treated HeLa or U937 cells .
0.5737 0.9998 0.9999 However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells , gave nearly wild-type levels of gene expression in phorbol ester -treated Jurkat cells but not in phorbol ester -treated cell_lineHeLa or U937 cells .
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3.9769 20.4971 10.9977 High level gene expression of these TAR mutant constructs in cell_linephorbol ester -treated Jurkat cells was eliminated by second site mutations in the enhancer region or by disruption of the tat gene .
2.8404 30.4043 10.1397 High level gene expression of these DNATAR mutant constructs in phorbol ester -treated Jurkat cells was eliminated by second site mutations in the enhancer region or by disruption of the tat gene .
2.1835 20.8546 0.9999 High level gene expression of these TAR mutant constructs in phorbol ester -treated Jurkat cells was eliminated by second site mutations in the DNAenhancer region or by disruption of the tat gene .
2.1746 20.8456 0.9999 High level gene expression of these TAR mutant constructs in phorbol ester -treated Jurkat cells was eliminated by second site mutations in the enhancer region or by disruption of the DNAtat gene .
0.8393 0.9990 0.9998 High level gene expression of these TAR mutant constructs in phorbol ester -treated cell_lineJurkat cells was eliminated by second site mutations in the enhancer region or by disruption of the tat gene .
1.8527 20.7963 0.9713 High level gene expression of these DNATAR mutant constructs in phorbol ester -treated Jurkat cells was eliminated by second site mutations in the enhancer region or by disruption of the tat gene .
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3.6495 20.0345 10.6092 A case of hypersensitivity to thyroid hormones with normally functioning thyroid gland and increased proteinnuclear triiodothyronine receptors .
A case of hypersensitivity to thyroid hormones with normally functioning thyroid gland and increased nuclear proteintriiodothyronine receptors .
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0.8757 1.0000 1.0000 The thyroid function was normal regarding T4 , free T4 and T3 , TBG , radioiodine uptake , TSH and T3 suppressibility ; however the proteinTSH response to TRH was decreased.
0.8491 1.0000 1.0000 The thyroid function was normal regarding T4 , free T4 and T3 , TBG , radioiodine uptake , proteinTSH and T3 suppressibility ; however the TSH response to TRH was decreased.
0.6378 1.0000 1.0000 The thyroid function was normal regarding T4 , free T4 and T3 , proteinTBG , radioiodine uptake , TSH and T3 suppressibility ; however the TSH response to TRH was decreased.
0.5941 1.0000 1.0000 The thyroid function was normal regarding T4 , free T4 and proteinT3 , TBG , radioiodine uptake , TSH and T3 suppressibility ; however the TSH response to TRH was decreased.
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1.7524 10.5990 0.9964 The proteinlymphocyte nuclear T3 receptor was found with an affinity close to that of normal volunteers (Ka: 1.42 x 10(10) M-1 vs 1.95 +/- 0.35 x 10(10) M-1) and a binding capacity markedly increased (9.9 vs 3.7 +/- 0.4 fmol T3 /100 micrograms DNA).
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0.8720 1.0000 0.9999 The clinical course and the laboratory data suggest that the tachycardia crises are the consequence of a hypersensitivity of the heart to thyroid hormones , associated with an increased number of T3 nuclear receptor sites in cell_typelymphocytes .
5.0949 30.0452 10.7801 The clinical course and the laboratory data suggest that the tachycardia crises are the consequence of a hypersensitivity of the heart to thyroid hormones , associated with an increased number of proteinT3 nuclear receptor sites in lymphocytes .
The clinical course and the laboratory data suggest that the tachycardia crises are the consequence of a hypersensitivity of the heart to thyroid hormones , associated with an increased number of proteinT3 nuclear receptor sites in lymphocytes .
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4.1173 20.1260 10.9325 Induction of DNAimmediate early response genes by macrophage colony-stimulating factor in normal human monocytes .
2.6985 10.9985 10.5257 Induction of immediate early response genes by proteinmacrophage colony-stimulating factor in normal human monocytes .
2.6281 10.7314 10.4283 Induction of immediate early response genes by macrophage colony-stimulating factor in cell_typenormal human monocytes .
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4.0872 20.5027 10.9768 A group of coordinately induced protooncogenes , cytoskeletal , and extracellular matrix genes have been termed DNAimmediate early response genes , and their induction has been associated with growth factor -stimulated cell proliferation .
1.7338 10.0214 1.0000 A group of coordinately induced DNAprotooncogenes , cytoskeletal , and extracellular matrix genes have been termed immediate early response genes , and their induction has been associated with growth factor -stimulated cell proliferation .
0.8300 0.9991 1.0000 A group of coordinately induced protooncogenes , cytoskeletal , and extracellular matrix genes have been termed immediate early response genes , and their induction has been associated with proteingrowth factor -stimulated cell proliferation .
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1.7483 10.3996 1.0000 We have investigated the induction of these genes by proteinmacrophage-CSF ( M-CSF ) in human monocytes that do not proliferate in response to M-CSF but require the factor for optimal cell differentiation .
1.7421 10.1455 1.0000 We have investigated the induction of these genes by macrophage-CSF ( M-CSF ) in human monocytes that do not proliferate in response to proteinM-CSF but require the factor for optimal cell differentiation .
1.6164 10.8554 0.9999 We have investigated the induction of these genes by macrophage-CSF ( M-CSF ) in cell_typehuman monocytes that do not proliferate in response to M-CSF but require the factor for optimal cell differentiation .
0.9886 1.0000 1.0000 We have investigated the induction of these genes by macrophage-CSF ( proteinM-CSF ) in human monocytes that do not proliferate in response to M-CSF but require the factor for optimal cell differentiation .
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0.8712 0.9919 0.9999 Normal cell_typehuman monocytes were isolated, carefully washed, and incubated for 36 to 48 h in fetal bovine serum-containing medium .
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2.3441 20.2990 1.0000 At the end of this incubation the cell_typeresting cells were stimulated with M-CSF , and RNA was isolated for analysis by Northern blotting .
1.8226 10.8230 1.0000 At the end of this incubation the resting cells were stimulated with M-CSF , and RNARNA was isolated for analysis by Northern blotting .
1.6637 10.4440 1.0000 At the end of this incubation the resting cells were stimulated with proteinM-CSF , and RNA was isolated for analysis by Northern blotting .
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2.3414 20.0256 0.9999 RNA from control resting cells contained low to undetectable levels of c-jun , fibronectin receptor , and RNAactin mRNA .
2.2283 20.1315 0.9999 RNA from control cell_typeresting cells contained low to undetectable levels of c-jun , fibronectin receptor , and actin mRNA .
0.8784 0.9997 1.0000 RNARNA from control resting cells contained low to undetectable levels of c-jun , fibronectin receptor , and actin mRNA .
1.4413 10.7613 1.0000 RNA from control resting cells contained low to undetectable levels of c-jun , proteinfibronectin receptor , and actin mRNA .
0.7529 0.9999 1.0000 RNA from control resting cells contained low to undetectable levels of DNAc-jun , fibronectin receptor , and actin mRNA .
RNA from control resting cells contained low to undetectable levels of c-jun , RNAfibronectin receptor , and actin mRNA .
RNA from control resting cells contained low to undetectable levels of RNAc-jun , fibronectin receptor , and actin mRNA .
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1.7262 10.9018 1.0000 Within 15 to 30 min of addition of proteinM-CSF , however, there was a dramatic coordinate induction of these genes.
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1.6483 10.8963 1.0000 The c-jun gene expression was very transient and was not detectable by 60 min after proteinM-CSF addition .
1.5933 10.4841 0.9999 The DNAc-jun gene expression was very transient and was not detectable by 60 min after M-CSF addition .
1.5446 10.7099 0.9758 The DNAc-jun gene expression was very transient and was not detectable by 60 min after M-CSF addition .
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0.9099 1.0000 1.0000 In contrast, the expression of actin and fibronectin receptor mRNA was more sustained, and the expression of these genes remained elevated at 24 to 48 h after proteinM-CSF addition .
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7.8940 30.6376 20.4483 We also observed the induction of the DNAmyelomonocytic specific tyrosine kinase hck gene simultaneously with the other immediate early response genes .
4.0904 20.5906 10.8853 We also observed the induction of the myelomonocytic specific tyrosine kinase hck gene simultaneously with the other DNAimmediate early response genes .
We also observed the induction of the proteinmyelomonocytic specific tyrosine kinase hck gene simultaneously with the other immediate early response genes .
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2.4713 20.2086 1.0000 The protein synthesis inhibitor cycloheximide did not block the induction of any of these genes, and in fact, super-induced the expression of DNAc-jun and hck .
0.8854 0.9999 1.0000 The protein synthesis inhibitor cycloheximide did not block the induction of any of these genes, and in fact, super-induced the expression of c-jun and DNAhck .
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2.2716 20.0583 1.0000 Nuclear run on transcription of the DNAc-jun , hck , and actin genes .
1.5017 10.4917 0.9998 Nuclear run on transcription of the c-jun , hck , and DNAactin genes .
0.8905 1.0000 1.0000 Nuclear run on transcription of the c-jun , DNAhck , and actin genes .
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3.0803 20.1305 10.8669 Therefore, in cell_typenormal human monocytes M-CSF induces immediate early response genes without inducing cell proliferation.
3.0640 10.5683 10.7831 Therefore, in normal human monocytes M-CSF induces DNAimmediate early response genes without inducing cell proliferation.
0.9355 0.9999 0.9999 Therefore, in normal human monocytes proteinM-CSF induces immediate early response genes without inducing cell proliferation.
Therefore, in normal cell_typehuman monocytes M-CSF induces immediate early response genes without inducing cell proliferation.
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0.9380 1.0000 1.0000 These genes may then play a role in altering the physiologic status of the cells in response to proteinCSF .
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4.5886 30.2139 10.8101 Inducible nuclear factor binding to the kappa B elements of the DNAhuman immunodeficiency virus enhancer in T cells can be blocked by cyclosporin A in a signal-dependent manner .
3.8004 20.5722 10.7602 Inducible nuclear factor binding to the DNAkappa B elements of the human immunodeficiency virus enhancer in T cells can be blocked by cyclosporin A in a signal-dependent manner .
1.5486 10.5303 0.9998 Inducible nuclear factor binding to the kappa B elements of the human immunodeficiency virus enhancer in cell_typeT cells can be blocked by cyclosporin A in a signal-dependent manner .
1.4089 0.9980 10.9769 proteinInducible nuclear factor binding to the kappa B elements of the human immunodeficiency virus enhancer in T cells can be blocked by cyclosporin A in a signal-dependent manner .
Inducible proteinnuclear factor binding to the kappa B elements of the human immunodeficiency virus enhancer in T cells can be blocked by cyclosporin A in a signal-dependent manner .
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2.5351 20.3857 1.0000 Cyclosporin A ( CsA ) is thought to exert its immunosuppressive effects by inhibiting the expression of a distinct set of DNAlymphokine genes which are induced upon T-cell activation , among them the gene coding for interleukin-2 .
1.7550 10.4091 1.0000 Cyclosporin A ( CsA ) is thought to exert its immunosuppressive effects by inhibiting the expression of a distinct set of lymphokine genes which are induced upon T-cell activation , among them the gene coding for proteininterleukin-2 .
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2.3760 20.3827 1.0000 To better understand the molecular mechanisms underlying suppression by CsA , we have investigated the effects of this drug on proteintranscription factors in T cells .
1.6807 10.9710 0.9998 To better understand the molecular mechanisms underlying suppression by CsA , we have investigated the effects of this drug on transcription factors in cell_typeT cells .
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3.6224 20.4711 10.9084 Here we report that the formation of two distinct proteinmitogen-inducible DNA-binding complexes , the kappa B complex within the HIV enhancer and the NFAT-1 complex within the interleukin-2 enhancer , is inhibited in the presence of CsA .
3.5829 20.1613 10.8089 Here we report that the formation of two distinct mitogen-inducible DNA-binding complexes , the proteinkappa B complex within the HIV enhancer and the NFAT-1 complex within the interleukin-2 enhancer , is inhibited in the presence of CsA .
2.2774 20.0319 0.9997 Here we report that the formation of two distinct mitogen-inducible DNA-binding complexes , the kappa B complex within the HIV enhancer and the NFAT-1 complex within the DNAinterleukin-2 enhancer , is inhibited in the presence of CsA .
2.2204 20.0906 1.0000 Here we report that the formation of two distinct mitogen-inducible DNA-binding complexes , the kappa B complex within the HIV enhancer and the proteinNFAT-1 complex within the interleukin-2 enhancer , is inhibited in the presence of CsA .
2.1842 20.0209 1.0000 Here we report that the formation of two distinct mitogen-inducible DNA-binding complexes , the kappa B complex within the DNAHIV enhancer and the NFAT-1 complex within the interleukin-2 enhancer , is inhibited in the presence of CsA .
Here we report that the formation of two distinct mitogen-inducible DNA-binding complexes , the kappa B complex within the HIV enhancer and the NFAT-1 complex within the proteininterleukin-2 enhancer , is inhibited in the presence of CsA .
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2.3320 20.4023 1.0000 The kappa B-binding activity with the DNAHIV enhancer is inhibited only if it is activated via the mitogen phytohemagglutinin whereas phorbol myristate acetate -mediated activation is completely insensitive to the drug.
0.6516 1.0000 1.0000 The kappa B-binding activity with the HIV enhancer is inhibited only if it is activated via the mitogen proteinphytohemagglutinin whereas phorbol myristate acetate -mediated activation is completely insensitive to the drug.
2.4720 20.3900 1.0000 The kappa B-binding activity with the HIV enhancer is inhibited only if it is activated via the proteinmitogen phytohemagglutinin whereas phorbol myristate acetate -mediated activation is completely insensitive to the drug.
The kappa B-binding activity with the HIV enhancer is inhibited only if it is activated via the proteinmitogen phytohemagglutinin whereas phorbol myristate acetate -mediated activation is completely insensitive to the drug.
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4.7978 20.8035 10.8040 This suggests a model in which functionally indistinguishable proteinkappa B complexes can be activated via two separate pathways of signal transduction distinguishable by CsA .
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5.6400 40.3900 10.8665 Purification of TCF-1 alpha , a T-cell-specific transcription factor that activates the DNAT-cell receptor C alpha gene enhancer in a context-dependent manner.
2.9558 20.6046 10.6665 Purification of TCF-1 alpha , a proteinT-cell-specific transcription factor that activates the T-cell receptor C alpha gene enhancer in a context-dependent manner.
1.7830 20.4589 1.0000 Purification of proteinTCF-1 alpha , a T-cell-specific transcription factor that activates the T-cell receptor C alpha gene enhancer in a context-dependent manner.
3.3327 40.5271 10.7139 Purification of TCF-1 alpha , a T-cell-specific transcription factor that activates the proteinT-cell receptor C alpha gene enhancer in a context-dependent manner.
1.0401 0.9998 10.4436 Purification of TCF-1 alpha , a T-cell-specific proteintranscription factor that activates the T-cell receptor C alpha gene enhancer in a context-dependent manner.
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2.4733 20.7436 0.9999 The differentiation of cell_typeT cells into functionally diverse subpopulations is controlled in part, by transcriptional activation and silencing ; however, little is known in detail about the proteins that influence this developmental process .
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3.6593 20.6674 10.6600 We have purified a new T-cell-specific factor , TCF-1 alpha , that is implicated in the activation of genes encoding a major component of the proteinhuman T-cell receptor ( TCR ).
2.0224 20.5133 0.9999 We have purified a new proteinT-cell-specific factor , TCF-1 alpha , that is implicated in the activation of genes encoding a major component of the human T-cell receptor ( TCR ).
1.6001 10.2170 1.0000 We have purified a new T-cell-specific factor , proteinTCF-1 alpha , that is implicated in the activation of genes encoding a major component of the human T-cell receptor ( TCR ).
0.9660 1.0000 1.0000 We have purified a new T-cell-specific factor , TCF-1 alpha , that is implicated in the activation of genes encoding a major component of the human T-cell receptor ( proteinTCR ).
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3.7466 20.7613 10.7106 TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the DNATCR alpha gene (e.g., p56lck and CD3 delta ).
3.6984 20.8326 10.6301 TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the DNATCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
1.5259 10.7507 1.0000 TCF-1 alpha , originally identified and purified through its binding sites on the DNAHIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
0.9385 1.0000 1.0000 proteinTCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
0.8785 1.0000 1.0000 TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to DNApromoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
2.2012 20.2896 0.9999 TCF-1 alpha , originally identified and purified through its DNAbinding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
0.8995 1.0000 1.0000 TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., proteinp56lck and CD3 delta ).
0.8395 10.6766 0.9999 TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and proteinCD3 delta ).
TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the proteinTCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., DNAp56lck and CD3 delta ).
TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several DNAgenes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and CD3 delta ).
TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the TCR alpha gene (e.g., p56lck and DNACD3 delta ).
TCF-1 alpha , originally identified and purified through its binding sites on the HIV-1 promoter , was found to bind to the TCR alpha enhancer and to promoters for several genes expressed at significantly earlier stages of T-cell development than the proteinTCR alpha gene (e.g., p56lck and CD3 delta ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7260 30.5243 10.6104 Sequences related to the DNATCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human TCR delta (and possibly TCR beta ) enhancers .
2.3791 30.3303 0.9823 Sequences related to the proteinTCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human TCR delta (and possibly TCR beta ) enhancers .
3.1732 20.9556 10.6076 Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human TCR delta (and possibly DNATCR beta ) enhancers .
Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human TCR delta (and possibly DNATCR beta ) enhancers .
Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the DNAhuman TCR delta (and possibly TCR beta ) enhancers .
Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human TCR delta (and possibly TCR beta ) DNAenhancers .
Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human proteinTCR delta (and possibly TCR beta ) enhancers .
Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human TCR delta (and possibly proteinTCR beta ) enhancers .
Sequences related to the TCF-1 alpha binding motif ( 5'-GGCACCCTTTGA-3' ) are also found in the human DNATCR delta (and possibly TCR beta ) enhancers .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5527 30.2227 10.4299 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of protein57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in mature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
3.8383 20.9062 10.7468 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in mature B cells ( JY , Namalwa ) or cell_linenonlymphoid (HeLa) cell lines .
1.5305 10.2454 1.0000 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that proteinTCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in mature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
0.9467 1.0000 1.0000 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in mature B cells ( cell_lineJY , Namalwa ) or nonlymphoid (HeLa) cell lines .
0.9418 1.0000 1.0000 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , cell_lineCCRF-CEM ) and not in mature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
0.9382 1.0000 1.0000 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in mature B cells ( JY , cell_lineNamalwa ) or nonlymphoid (HeLa) cell lines .
0.9227 1.0000 1.0000 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( cell_lineJurkat , CCRF-CEM ) and not in mature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
4.1820 20.8495 10.4860 Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in cell_typemature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
3.7084 20.9562 10.3982 Southwestern and gel renaturation experiments with the use of proteinpurified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in mature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
Southwestern and gel renaturation experiments with the use of purified protein fractions revealed that TCF-1 alpha activity is derived from a family of 57- to 53-kD proteins that are abundantly expressed in mature and immature T-cell lines ( Jurkat , CCRF-CEM ) and not in cell_linemature B cells ( JY , Namalwa ) or nonlymphoid (HeLa) cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6671 20.8476 10.9446 A small 95-bp fragment of the TCR alpha control region that contains the DNATCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
4.3478 20.9826 10.5387 A small 95-bp fragment of the DNATCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
3.8198 20.0609 10.8387 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or DNAT alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
1.9941 20.8335 0.9999 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent DNAT-cell-specific enhancer in vivo.
1.9269 20.1585 0.9999 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a DNAcAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
1.8949 20.7261 0.9419 A small 95-bp fragment of the TCR alpha control region that contains the proteinTCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
1.4510 10.6238 1.0000 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct proteinlymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
1.2491 10.2741 0.9997 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the DNAbinding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
0.8668 1.0000 1.0000 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the DNACRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
0.8167 0.9998 1.0000 A small 95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( proteinTCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
2.0664 20.7225 0.9999 A small DNA95-bp fragment of the TCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
A small 95-bp fragment of the proteinTCR alpha control region that contains the TCF-1 alpha binding site juxtaposed between a cAMP-response element (the CRE or T alpha 1 motif ) and the binding site for a distinct lymphoid-specific protein ( TCF-2 alpha ) behaved as a potent T-cell-specific enhancer in vivo.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1110 10.9080 10.8387 Tandem copies of this enhancer functioned synergistically in cell_linemature (Jurkat) T-cell lines as well as resting and activated immature (CCRF-CEM) T-cell lines .
2.8507 10.9349 10.9051 Tandem copies of this enhancer functioned synergistically in mature (Jurkat) T-cell lines as well as resting and cell_lineactivated immature (CCRF-CEM) T-cell lines .
0.7188 1.0000 1.0000 Tandem copies of this DNAenhancer functioned synergistically in mature (Jurkat) T-cell lines as well as resting and activated immature (CCRF-CEM) T-cell lines .
Tandem copies of this enhancer functioned synergistically in mature (Jurkat) T-cell lines as well as resting and activated cell_lineimmature (CCRF-CEM) T-cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9200 20.7034 10.6120 Mutation of the DNATCF-1 alpha binding site diminished enhancer activity and disrupted the synergism observed in vivo between tandem enhancer repeats .
3.3961 20.9105 10.6227 Mutation of the TCF-1 alpha binding site diminished enhancer activity and disrupted the synergism observed in vivo between DNAtandem enhancer repeats .
1.8406 20.7959 0.9626 Mutation of the proteinTCF-1 alpha binding site diminished enhancer activity and disrupted the synergism observed in vivo between tandem enhancer repeats .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8029 20.9447 10.6107 The TCF-1 alpha binding site was also required for TCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not HeLa cells , confirming that TCF-1 alpha is a proteinT-cell-specific transcription factor .
2.3938 10.3493 10.0496 The DNATCF-1 alpha binding site was also required for TCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not HeLa cells , confirming that TCF-1 alpha is a T-cell-specific transcription factor .
1.6047 10.3821 1.0000 The TCF-1 alpha binding site was also required for TCR alpha enhancer activity in transcriptionally active extracts from cell_lineJurkat but not HeLa cells , confirming that TCF-1 alpha is a T-cell-specific transcription factor .
1.4169 10.9917 1.0000 The TCF-1 alpha binding site was also required for TCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not HeLa cells , confirming that proteinTCF-1 alpha is a T-cell-specific transcription factor .
1.4011 10.5772 0.9998 The TCF-1 alpha binding site was also required for TCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not cell_lineHeLa cells , confirming that TCF-1 alpha is a T-cell-specific transcription factor .
1.2861 10.4171 0.7552 The proteinTCF-1 alpha binding site was also required for TCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not HeLa cells , confirming that TCF-1 alpha is a T-cell-specific transcription factor .
3.4546 20.4041 10.9241 The TCF-1 alpha binding site was also required for DNATCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not HeLa cells , confirming that TCF-1 alpha is a T-cell-specific transcription factor .
The TCF-1 alpha binding site was also required for proteinTCR alpha enhancer activity in transcriptionally active extracts from Jurkat but not HeLa cells , confirming that TCF-1 alpha is a T-cell-specific transcription factor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4847 20.8644 10.5713 Curiously, the TCF-1 alpha binding element was inactive in vivo when removed from its neighboring elements on the DNATCR alpha enhancer and positioned in one or more copies upstream of a heterologous promoter .
2.0336 20.9452 0.9999 Curiously, the TCF-1 alpha binding element was inactive in vivo when removed from its neighboring elements on the TCR alpha enhancer and positioned in one or more copies upstream of a DNAheterologous promoter .
2.0236 20.9423 0.9234 Curiously, the proteinTCF-1 alpha binding element was inactive in vivo when removed from its neighboring elements on the TCR alpha enhancer and positioned in one or more copies upstream of a heterologous promoter .
3.2512 20.9481 10.4034 Curiously, the DNATCF-1 alpha binding element was inactive in vivo when removed from its neighboring elements on the TCR alpha enhancer and positioned in one or more copies upstream of a heterologous promoter .
Curiously, the TCF-1 alpha binding element was inactive in vivo when removed from its neighboring elements on the proteinTCR alpha enhancer and positioned in one or more copies upstream of a heterologous promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4898 20.5333 10.0562 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) transcription factors and the context of its binding site within the DNATCR alpha enhancer .
1.8048 20.9855 0.9998 Thus, the transcriptional activity of proteinTCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) transcription factors and the context of its binding site within the TCR alpha enhancer .
1.5370 20.2946 0.9718 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the proteinTCF-2 alpha and T alpha 1 ( CREB ) transcription factors and the context of its binding site within the TCR alpha enhancer .
0.9462 1.0000 0.9843 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( proteinCREB ) transcription factors and the context of its binding site within the TCR alpha enhancer .
0.5928 0.6259 0.9965 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) proteintranscription factors and the context of its binding site within the TCR alpha enhancer .
1.6741 20.1656 0.9997 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) transcription factors and the context of its DNAbinding site within the TCR alpha enhancer .
1.5777 0.9606 20.9651 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the proteinTCF-2 alpha and T alpha 1 ( CREB ) transcription factors and the context of its binding site within the TCR alpha enhancer .
0.6646 1.0000 0.9844 Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and proteinT alpha 1 ( CREB ) transcription factors and the context of its binding site within the TCR alpha enhancer .
Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) transcription factors and the context of its binding site within the proteinTCR alpha enhancer .
Thus, the transcriptional activity of TCF-1 alpha appears to depend on the TCF-2 alpha and proteinT alpha 1 ( CREB ) transcription factors and the context of its binding site within the TCR alpha enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.6922 30.4532 20.2512 Tandem AP-1-binding sites within the DNAhuman beta-globin dominant control region function as an inducible enhancer in erythroid cells .
1.7436 20.1464 0.9996 Tandem AP-1-binding sites within the human beta-globin dominant control region function as an DNAinducible enhancer in erythroid cells .
1.4735 0.9972 10.7146 DNATandem AP-1-binding sites within the human beta-globin dominant control region function as an inducible enhancer in erythroid cells .
1.2178 10.3898 0.9990 Tandem AP-1-binding sites within the human beta-globin dominant control region function as an inducible enhancer in cell_typeerythroid cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1384 20.2575 10.9778 A powerful enhancer has been mapped to an DNA18-bp DNA segment located 11 kb 5' to the human epsilon-globin gene within the dominant control or locus-activating region .
2.7516 10.8935 10.7482 A powerful enhancer has been mapped to an 18-bp DNA segment located 11 kb 5' to the DNAhuman epsilon-globin gene within the dominant control or locus-activating region .
1.3838 10.8533 0.9997 A powerful enhancer has been mapped to an 18-bp DNA segment located 11 kb 5' to the human epsilon-globin gene within the dominant control or DNAlocus-activating region .
2.1285 10.8283 10.1697 A powerful enhancer has been mapped to an 18-bp DNA segment located DNA11 kb 5' to the human epsilon-globin gene within the dominant control or locus-activating region .
1.6282 10.4153 1.0000 A powerful DNAenhancer has been mapped to an 18-bp DNA segment located 11 kb 5' to the human epsilon-globin gene within the dominant control or locus-activating region .
A powerful enhancer has been mapped to an 18-bp DNA segment located 11 kb 5' to the human epsilon-globin gene within the DNAdominant control or locus-activating region .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6503 20.9002 10.8859 This enhancer is inducible in cell_lineK562 human erythroleukemia cells , increasing linked gamma-globin promoter /luciferase gene expression to 170-fold over an enhancerless construct .
1.8748 20.6221 0.9997 This enhancer is inducible in K562 human erythroleukemia cells , increasing linked gamma-globin promoter /luciferase gene expression to 170-fold over an DNAenhancerless construct .
1.8253 20.9020 0.9456 This enhancer is inducible in K562 human erythroleukemia cells , increasing linked DNAgamma-globin promoter /luciferase gene expression to 170-fold over an enhancerless construct .
0.8268 0.9998 1.0000 This DNAenhancer is inducible in K562 human erythroleukemia cells , increasing linked gamma-globin promoter /luciferase gene expression to 170-fold over an enhancerless construct .
3.8810 20.9508 10.1975 This enhancer is inducible in K562 human erythroleukemia cells , increasing linked DNAgamma-globin promoter /luciferase gene expression to 170-fold over an enhancerless construct .
This enhancer is inducible in K562 human erythroleukemia cells , increasing linked gamma-globin promoter protein/luciferase gene expression to 170-fold over an enhancerless construct .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9213 1.0000 1.0000 The DNAenhancer consists of tandem AP-1-binding sites , phased 10 bp apart, which are both required for full activity.
2.3913 20.1718 0.9999 The enhancer consists of tandem DNAAP-1-binding sites , phased 10 bp apart, which are both required for full activity.
The enhancer consists of DNAtandem AP-1-binding sites , phased 10 bp apart, which are both required for full activity.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5663 20.1593 10.6332 DNA-protein binding assays with nuclear extracts from induced cells demonstrate a proteinhigh molecular weight complex on the enhancer .
1.5777 10.5973 1.0000 DNA-protein binding assays with nuclear extracts from induced cells demonstrate a high molecular weight complex on the DNAenhancer .
1.9573 20.1269 0.9999 DNA-protein binding assays with nuclear extracts from cell_typeinduced cells demonstrate a high molecular weight complex on the enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6173 10.9810 1.0000 The formation of this complex also requires both DNAAP-1 sites and correlates with maximal enhancer activity .
The formation of this complex also requires both AP-1 sites and correlates with maximal DNAenhancer activity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4430 20.5821 1.0000 Induction of the enhancer may have a role in the increase in DNAglobin gene transcription that characterizes erythroid maturation .
1.5588 10.5281 1.0000 Induction of the DNAenhancer may have a role in the increase in globin gene transcription that characterizes erythroid maturation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7342 20.8979 10.5153 Enhancer activity appears to be mediated by the binding of a complex of proteins from the jun and fos families to DNAtandem AP-1 consensus sequences .
Enhancer activity appears to be mediated by the binding of a complex of proteins from the DNAjun and fos families to tandem AP-1 consensus sequences .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1680 30.1393 10.7497 Identification of a novel factor that interacts with an immunoglobulin heavy-chain promoter and stimulates transcription in conjunction with the proteinlymphoid cell-specific factor OTF2 .
3.5261 20.8821 10.6941 Identification of a novel factor that interacts with an DNAimmunoglobulin heavy-chain promoter and stimulates transcription in conjunction with the lymphoid cell-specific factor OTF2 .
2.0310 20.4799 0.9999 Identification of a proteinnovel factor that interacts with an immunoglobulin heavy-chain promoter and stimulates transcription in conjunction with the lymphoid cell-specific factor OTF2 .
0.9559 0.9999 1.0000 Identification of a novel factor that interacts with an immunoglobulin heavy-chain promoter and stimulates transcription in conjunction with the lymphoid cell-specific factor proteinOTF2 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4432 20.9336 10.9922 The tissue-specific expression of the DNAMOPC 141 immunoglobulin heavy-chain gene was studied by using in vitro transcription .
1.4192 0.9969 10.7822 The tissue-specific expression of the MOPC 141 DNAimmunoglobulin heavy-chain gene was studied by using in vitro transcription .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1540 20.7358 0.9995 B-cell-specific transcription of this gene was dependent on the DNAoctamer element 5'-ATGCAAAG-3' , located in the upstream region of this promoter and in the promoters of all other immunoglobulin heavy- and light- chain genes .
1.4685 10.8526 0.9999 B-cell-specific transcription of this gene was dependent on the octamer element 5'-ATGCAAAG-3' , located in the DNAupstream region of this promoter and in the promoters of all other immunoglobulin heavy- and light- chain genes .
0.9130 1.0000 1.0000 B-cell-specific transcription of this gene was dependent on the octamer element 5'-ATGCAAAG-3' , located in the upstream region of this promoter and in the DNApromoters of all other immunoglobulin heavy- and light- chain genes .
0.9130 1.0000 1.0000 B-cell-specific transcription of this gene was dependent on the octamer element 5'-ATGCAAAG-3' , located in the upstream region of this DNApromoter and in the promoters of all other immunoglobulin heavy- and light- chain genes .
5.3699 20.9079 20.4615 B-cell-specific transcription of this gene was dependent on the octamer element 5'-ATGCAAAG-3' , located in the upstream region of this promoter and in the promoters of all other DNAimmunoglobulin heavy- and light- chain genes .
0.7793 0.9998 1.0000 B-cell-specific transcription of this gene was dependent on the octamer element DNA5'-ATGCAAAG-3' , located in the upstream region of this promoter and in the promoters of all other immunoglobulin heavy- and light- chain genes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4818 20.9387 10.9587 The interaction of purified octamer transcription factors 1 and 2 ( OTF1 and OTF2 ) with the DNAMOPC 141 promoter was studied by using electrophoretic mobility shift assays and DNase I footprinting .
2.0519 20.2004 0.9999 The interaction of purified octamer transcription factors 1 and 2 ( OTF1 and OTF2 ) with the MOPC 141 promoter was studied by using electrophoretic mobility shift assays and proteinDNase I footprinting .
0.9641 1.0000 1.0000 The interaction of purified octamer transcription factors 1 and 2 ( OTF1 and proteinOTF2 ) with the MOPC 141 promoter was studied by using electrophoretic mobility shift assays and DNase I footprinting .
0.9456 1.0000 1.0000 The interaction of purified octamer transcription factors 1 and 2 ( proteinOTF1 and OTF2 ) with the MOPC 141 promoter was studied by using electrophoretic mobility shift assays and DNase I footprinting .
0.5377 0.9982 0.9996 The interaction of purified octamer proteintranscription factors 1 and 2 ( OTF1 and OTF2 ) with the MOPC 141 promoter was studied by using electrophoretic mobility shift assays and DNase I footprinting .
5.2719 30.0278 10.5426 The interaction of proteinpurified octamer transcription factors 1 and 2 ( OTF1 and OTF2 ) with the MOPC 141 promoter was studied by using electrophoretic mobility shift assays and DNase I footprinting .
The interaction of purified proteinoctamer transcription factors 1 and 2 ( OTF1 and OTF2 ) with the MOPC 141 promoter was studied by using electrophoretic mobility shift assays and DNase I footprinting .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1957 20.9624 0.9999 Purified OTF1 from HeLa cells and OTF1 and OTF2 from B cells bound to identical sequences within the DNAheavy-chain promoter .
1.7207 10.2083 1.0000 Purified proteinOTF1 from HeLa cells and OTF1 and OTF2 from B cells bound to identical sequences within the heavy-chain promoter .
1.5456 10.3825 0.9998 Purified OTF1 from HeLa cells and OTF1 and OTF2 from cell_typeB cells bound to identical sequences within the heavy-chain promoter .
1.5283 10.8293 0.9998 Purified OTF1 from cell_lineHeLa cells and OTF1 and OTF2 from B cells bound to identical sequences within the heavy-chain promoter .
0.9518 1.0000 1.0000 Purified OTF1 from HeLa cells and OTF1 and proteinOTF2 from B cells bound to identical sequences within the heavy-chain promoter .
0.9275 1.0000 1.0000 Purified OTF1 from HeLa cells and proteinOTF1 and OTF2 from B cells bound to identical sequences within the heavy-chain promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2650 20.8375 0.9996 The OTF interactions we observed extended over the DNAheptamer element 5'-CTCAGGA-3' , and it seems likely that the binding of the purified factors involves cooperation between octamer and heptamer sites in this promoter .
2.2463 20.3306 1.0000 The OTF interactions we observed extended over the heptamer element 5'-CTCAGGA-3' , and it seems likely that the binding of the proteinpurified factors involves cooperation between octamer and heptamer sites in this promoter .
1.7858 10.2775 1.0000 The OTF interactions we observed extended over the heptamer element 5'-CTCAGGA-3' , and it seems likely that the binding of the purified factors involves cooperation between octamer and heptamer sites in this DNApromoter .
1.5802 10.3593 1.0000 The OTF interactions we observed extended over the heptamer element 5'-CTCAGGA-3' , and it seems likely that the binding of the purified factors involves cooperation between octamer and DNAheptamer sites in this promoter .
0.9156 1.0000 1.0000 The proteinOTF interactions we observed extended over the heptamer element 5'-CTCAGGA-3' , and it seems likely that the binding of the purified factors involves cooperation between octamer and heptamer sites in this promoter .
0.8925 0.9999 1.0000 The OTF interactions we observed extended over the heptamer element DNA5'-CTCAGGA-3' , and it seems likely that the binding of the purified factors involves cooperation between octamer and heptamer sites in this promoter .
0.8843 1.0000 1.0000 The OTF interactions we observed extended over the heptamer element 5'-CTCAGGA-3' , and it seems likely that the binding of the purified factors involves cooperation between DNAoctamer and heptamer sites in this promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2601 20.1730 0.9999 In addition to these elements, we identified a second DNAregulatory element , the N element with the sequence 5'-GGAACCTCCCCC-3' .
1.5428 10.6488 1.0000 In addition to these elements, we identified a second regulatory element , the DNAN element with the sequence 5'-GGAACCTCCCCC-3' .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4340 20.2322 1.0000 The N element could independently mediate low levels of transcription in both B-cell and HeLa-cell extracts , and, in conjunction with the DNAoctamer element , it can promote high levels of transcription in B-cell extracts .
1.6679 10.9033 1.0000 The DNAN element could independently mediate low levels of transcription in both B-cell and HeLa-cell extracts , and, in conjunction with the octamer element , it can promote high levels of transcription in B-cell extracts .
1.5547 10.8856 0.9997 The N element could independently mediate low levels of transcription in both B-cell and HeLa-cell extracts , and, in conjunction with the octamer element , it can promote high levels of transcription in cell_typeB-cell extracts .
0.6017 0.9998 0.9999 The N element could independently mediate low levels of transcription in both B-cell and cell_lineHeLa-cell extracts , and, in conjunction with the octamer element , it can promote high levels of transcription in B-cell extracts .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6312 10.8649 0.9999 The DNAN element bound a transcription factor , NTF , that is ubiquitous in cell-type distribution , and NTF was distinct from any of the previously described proteins that bind to similar sequences.
1.5389 10.6321 1.0000 The N element bound a proteintranscription factor , NTF , that is ubiquitous in cell-type distribution , and NTF was distinct from any of the previously described proteins that bind to similar sequences.
0.9495 1.0000 1.0000 The N element bound a transcription factor , proteinNTF , that is ubiquitous in cell-type distribution , and NTF was distinct from any of the previously described proteins that bind to similar sequences.
0.9184 1.0000 1.0000 The N element bound a transcription factor , NTF , that is ubiquitous in cell-type distribution , and proteinNTF was distinct from any of the previously described proteins that bind to similar sequences.
The N element bound a transcription factor , NTF , that is ubiquitous in proteincell-type distribution , and NTF was distinct from any of the previously described proteins that bind to similar sequences.
The N element bound a transcription factor , NTF , that is ubiquitous in cell-type distribution , and NTF was distinct from any of the proteinpreviously described proteins that bind to similar sequences.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8677 20.6418 10.6470 Based on these results, we propose that NTF and OTF2 interactions (both with their DNAcognate DNA elements and possibly at the protein-protein level ) may be critical to B-cell-specific expression and that these interactions provide additional pathways for regulating gene expression .
0.9687 1.0000 1.0000 Based on these results, we propose that NTF and proteinOTF2 interactions (both with their cognate DNA elements and possibly at the protein-protein level ) may be critical to B-cell-specific expression and that these interactions provide additional pathways for regulating gene expression .
0.9252 1.0000 1.0000 Based on these results, we propose that proteinNTF and OTF2 interactions (both with their cognate DNA elements and possibly at the protein-protein level ) may be critical to B-cell-specific expression and that these interactions provide additional pathways for regulating gene expression .
0.6752 0.9999 0.9999 Based on these results, we propose that NTF and OTF2 interactions (both with their cognate DNADNA elements and possibly at the protein-protein level ) may be critical to B-cell-specific expression and that these interactions provide additional pathways for regulating gene expression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.0998 30.1762 20.1792 NF-kappa B as inducible transcriptional activator of the DNAgranulocyte-macrophage colony-stimulating factor gene .
0.8771 0.9999 1.0000 proteinNF-kappa B as inducible transcriptional activator of the granulocyte-macrophage colony-stimulating factor gene .
NF-kappa B as inducible proteintranscriptional activator of the granulocyte-macrophage colony-stimulating factor gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6848 20.6207 10.3969 The expression of the gene encoding the proteingranulocyte- macrophage colony-stimulating factor ( GM-CSF ) is induced upon activation of T cells with phytohemagglutinin and active phorbolester and upon expression of tax1 , a transactivating protein of the human T-cell leukemia virus type I .
2.3550 20.5247 0.9999 The expression of the gene encoding the granulocyte- macrophage colony-stimulating factor ( GM-CSF ) is induced upon activation of cell_typeT cells with phytohemagglutinin and active phorbolester and upon expression of tax1 , a transactivating protein of the human T-cell leukemia virus type I .
1.7484 10.0079 1.0000 The expression of the gene encoding the granulocyte- macrophage colony-stimulating factor ( GM-CSF ) is induced upon activation of T cells with proteinphytohemagglutinin and active phorbolester and upon expression of tax1 , a transactivating protein of the human T-cell leukemia virus type I .
1.6416 10.9409 1.0000 The expression of the gene encoding the granulocyte- macrophage colony-stimulating factor ( GM-CSF ) is induced upon activation of T cells with phytohemagglutinin and active phorbolester and upon expression of proteintax1 , a transactivating protein of the human T-cell leukemia virus type I .
1.5482 10.1856 0.9999 The expression of the gene encoding the granulocyte- macrophage colony-stimulating factor ( GM-CSF ) is induced upon activation of T cells with phytohemagglutinin and active phorbolester and upon expression of tax1 , a proteintransactivating protein of the human T-cell leukemia virus type I .
0.9781 1.0000 1.0000 The expression of the gene encoding the granulocyte- macrophage colony-stimulating factor ( proteinGM-CSF ) is induced upon activation of T cells with phytohemagglutinin and active phorbolester and upon expression of tax1 , a transactivating protein of the human T-cell leukemia virus type I .
The expression of the gene encoding the granulocyte- proteinmacrophage colony-stimulating factor ( GM-CSF ) is induced upon activation of T cells with phytohemagglutinin and active phorbolester and upon expression of tax1 , a transactivating protein of the human T-cell leukemia virus type I .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8150 20.7154 10.6720 The same agents induce transcription from the interleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the inducible transcription factor NF-kappa B (or an proteinNF-kappa B -like factor ).
2.0301 20.2280 0.9732 The same agents induce transcription from the interleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the inducible transcription factor NF-kappa B (or an proteinNF-kappa B -like factor ).
1.3790 10.9269 0.9998 The same agents induce transcription from the interleukin-2 receptor alpha-chain and interleukin-2 genes , depending on DNApromoter elements that bind the inducible transcription factor NF-kappa B (or an NF-kappa B -like factor ).
0.8786 0.9986 0.9999 The same agents induce transcription from the interleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the inducible transcription factor proteinNF-kappa B (or an NF-kappa B -like factor ).
3.4847 20.8460 10.7448 The same agents induce transcription from the proteininterleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the inducible transcription factor NF-kappa B (or an NF-kappa B -like factor ).
1.9945 20.1564 0.9966 The same agents induce transcription from the proteininterleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the inducible transcription factor NF-kappa B (or an NF-kappa B -like factor ).
1.4562 10.6980 0.9999 The same agents induce transcription from the interleukin-2 receptor alpha-chain and DNAinterleukin-2 genes , depending on promoter elements that bind the inducible transcription factor NF-kappa B (or an NF-kappa B -like factor ).
1.4105 10.6359 0.9995 The same agents induce transcription from the interleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the inducible proteintranscription factor NF-kappa B (or an NF-kappa B -like factor ).
The same agents induce transcription from the interleukin-2 receptor alpha-chain and interleukin-2 genes , depending on promoter elements that bind the proteininducible transcription factor NF-kappa B (or an NF-kappa B -like factor ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0992 20.7710 0.9996 We therefore tested the possibility that the GM-CSF gene is also regulated by a cognate motif for the proteinNF-kappa B transcription factor .
2.0588 20.7360 1.0000 We therefore tested the possibility that the DNAGM-CSF gene is also regulated by a cognate motif for the NF-kappa B transcription factor .
1.9184 20.7951 0.9883 We therefore tested the possibility that the proteinGM-CSF gene is also regulated by a cognate motif for the NF-kappa B transcription factor .
1.9094 20.6605 0.9954 We therefore tested the possibility that the GM-CSF gene is also regulated by a cognate motif for the proteinNF-kappa B transcription factor .
0.8766 0.9990 0.9998 We therefore tested the possibility that the GM-CSF gene is also regulated by a cognate motif for the NF-kappa B proteintranscription factor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3023 30.2790 10.3731 A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a short promoter region in the GM-CSF gene that conferred strong inducibility by T-cell-activating signals and tax1 , but no DNANF-kappa B -binding motifs were identified.
2.2191 20.6996 1.0000 A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a short promoter region in the DNAGM-CSF gene that conferred strong inducibility by T-cell-activating signals and tax1 , but no NF-kappa B -binding motifs were identified.
2.1225 20.0629 0.9589 A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a short promoter region in the GM-CSF gene that conferred strong inducibility by T-cell-activating signals and tax1 , but no proteinNF-kappa B -binding motifs were identified.
2.0372 20.9234 0.9920 A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a short promoter region in the proteinGM-CSF gene that conferred strong inducibility by T-cell-activating signals and tax1 , but no NF-kappa B -binding motifs were identified.
1.6402 10.9902 1.0000 A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a short promoter region in the GM-CSF gene that conferred strong inducibility by T-cell-activating signals and proteintax1 , but no NF-kappa B -binding motifs were identified.
2.2504 20.6176 0.9999 A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a short DNApromoter region in the GM-CSF gene that conferred strong inducibility by T-cell-activating signals and tax1 , but no NF-kappa B -binding motifs were identified.
A recent functional analysis by Miyatake et al. (S. Miyatake, M. Seiki, M. Yoshida, and K. Arai, Mol. Cell. Biol. 8:5581-5587, 1988) described a DNAshort promoter region in the GM-CSF gene that conferred strong inducibility by T-cell-activating signals and tax1 , but no NF-kappa B -binding motifs were identified.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.4517 20.3441 10.7520 Using electrophoretic mobility shift assays , we showed binding of purified human NF-kappa B and of the NF-kappa B activated in cell_lineJurkat T cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
3.0537 20.8388 10.5741 Using electrophoretic mobility shift assays , we showed binding of purified human NF-kappa B and of the NF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the DNAGM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
1.9986 20.0737 0.9967 Using electrophoretic mobility shift assays , we showed binding of purified human NF-kappa B and of the NF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the proteinGM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
1.4869 10.8160 1.0000 Using electrophoretic mobility shift assays , we showed binding of purified human NF-kappa B and of the proteinNF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
1.4353 10.4535 1.0000 Using electrophoretic mobility shift assays , we showed binding of purified human NF-kappa B and of the NF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and proteintax1 .
0.9078 0.9998 1.0000 Using electrophoretic mobility shift assays , we showed binding of purified human proteinNF-kappa B and of the NF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
4.0037 20.7773 10.9340 Using electrophoretic mobility shift assays , we showed binding of proteinpurified human NF-kappa B and of the NF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
Using electrophoretic mobility shift assays , we showed binding of purified human NF-kappa B and of the NF-kappa B activated in Jurkat cell_typeT cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
Using electrophoretic mobility shift assays , we showed binding of purified proteinhuman NF-kappa B and of the NF-kappa B activated in Jurkat T cells to an oligonucleotide comprising the GM-CSF promoter element responsible for mediating responsiveness to T-cell-activating signals and tax1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.4069 30.7928 10.7856 As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the DNAbeta interferon promoter ( GGGAAATTCC ).
0.7958 1.0000 1.0000 As shown by a methylation interference analysis and oligonucleotide competition experiments, purified proteinNF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
4.5961 20.8936 10.6603 As shown by a methylation interference analysis and oligonucleotide competition experiments, proteinpurified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
4.4144 20.5154 10.9281 As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions DNA-82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
3.7365 20.6228 10.5942 As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the DNAGM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
3.6374 20.9186 10.7821 As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional DNAkappa B motif in the beta interferon promoter ( GGGAAATTCC ).
As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the proteinGM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the DNAbiologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at positions -82 to -91 ( GGGAACTACC ) of the DNAGM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
As shown by a methylation interference analysis and oligonucleotide competition experiments, purified NF-kappa B binds at DNApositions -82 to -91 ( GGGAACTACC ) of the GM-CSF promoter sequence with an affinity similar to that with which it binds to the biologically functional kappa B motif in the beta interferon promoter ( GGGAAATTCC ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.7481 10.9692 10.6344 Two DNAkappa B-like motifs at positions -98 to -108 of the GM-CSF promoter were also recognized but with much lower affinities.
1.4071 10.8294 1.0000 Two kappa B-like motifs at positions -98 to -108 of the DNAGM-CSF promoter were also recognized but with much lower affinities.
2.9650 10.8475 10.5471 Two kappa B-like motifs at positions DNA-98 to -108 of the GM-CSF promoter were also recognized but with much lower affinities.
Two kappa B-like motifs at positions -98 to -108 of the proteinGM-CSF promoter were also recognized but with much lower affinities.
Two kappa B-like motifs at DNApositions -98 to -108 of the GM-CSF promoter were also recognized but with much lower affinities.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6115 20.4646 10.6479 Our data provide strong evidence that the expression of the GM-CSF gene following T-cell activation is controlled by binding of the NF-kappa B transcription factor to a DNAhigh-affinity binding site in the GM-CSF promoter .
2.1301 20.1359 0.9995 Our data provide strong evidence that the expression of the GM-CSF gene following T-cell activation is controlled by binding of the proteinNF-kappa B transcription factor to a high-affinity binding site in the GM-CSF promoter .
2.1143 20.8672 1.0000 Our data provide strong evidence that the expression of the DNAGM-CSF gene following T-cell activation is controlled by binding of the NF-kappa B transcription factor to a high-affinity binding site in the GM-CSF promoter .
2.0838 20.5011 0.9998 Our data provide strong evidence that the expression of the GM-CSF gene following T-cell activation is controlled by binding of the NF-kappa B transcription factor to a high-affinity binding site in the DNAGM-CSF promoter .
1.9799 20.8586 0.9904 Our data provide strong evidence that the expression of the proteinGM-CSF gene following T-cell activation is controlled by binding of the NF-kappa B transcription factor to a high-affinity binding site in the GM-CSF promoter .
1.9446 20.9526 0.9863 Our data provide strong evidence that the expression of the GM-CSF gene following T-cell activation is controlled by binding of the NF-kappa B transcription factor to a high-affinity binding site in the proteinGM-CSF promoter .
0.8584 0.9963 0.9999 Our data provide strong evidence that the expression of the GM-CSF gene following T-cell activation is controlled by binding of the NF-kappa B proteintranscription factor to a high-affinity binding site in the GM-CSF promoter .
Our data provide strong evidence that the expression of the GM-CSF gene following T-cell activation is controlled by binding of the proteinNF-kappa B transcription factor to a high-affinity binding site in the GM-CSF promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6657 20.5457 20.0060 Effects of mitogenic agents upon glucocorticoid action in cell_typehuman tonsillar T- lymphocytes .
1.7001 20.3272 10.7488 Effects of mitogenic agents upon glucocorticoid action in cell_typehuman tonsillar T- lymphocytes .
Effects of mitogenic agents upon glucocorticoid action in human tonsillar T- cell_typelymphocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0129 20.2382 20.2375 The treatment of cell_typehuman tonsillar T- lymphocytes with 4-phorbol 12-myristate 13-acetate ( PMA ), resulted in about two fold increase in glucocorticoid receptor ( GR ) number , without any significant change in the receptor affinity .
2.2927 20.9990 1.0000 The treatment of human tonsillar T- lymphocytes with 4-phorbol 12-myristate 13-acetate ( PMA ), resulted in about two fold increase in proteinglucocorticoid receptor ( GR ) number , without any significant change in the receptor affinity .
0.9810 1.0000 1.0000 The treatment of human tonsillar T- lymphocytes with 4-phorbol 12-myristate 13-acetate ( PMA ), resulted in about two fold increase in glucocorticoid receptor ( proteinGR ) number , without any significant change in the receptor affinity .
1.9532 20.3622 10.8130 The treatment of cell_typehuman tonsillar T- lymphocytes with 4-phorbol 12-myristate 13-acetate ( PMA ), resulted in about two fold increase in glucocorticoid receptor ( GR ) number , without any significant change in the receptor affinity .
The treatment of human tonsillar T- cell_typelymphocytes with 4-phorbol 12-myristate 13-acetate ( PMA ), resulted in about two fold increase in glucocorticoid receptor ( GR ) number , without any significant change in the receptor affinity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6222 10.9185 1.0000 Alone, PMA and calcium ionophore A23187 did not affect, but together stimulated, like proteinphytohaemagglutinin ( PHA ), leucine and, in particular, thymidine incorporation .
0.9724 1.0000 1.0000 Alone, PMA and calcium ionophore A23187 did not affect, but together stimulated, like phytohaemagglutinin ( proteinPHA ), leucine and, in particular, thymidine incorporation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5478 10.8205 1.0000 PMA enhanced slightly the stimulatory effect of proteinPHA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9180 1.0000 1.0000 Alone, these agents failed to alter the suppressive effect of dexamethasone on thymidine and leucine incorporation ; however, PMA -A23187 and PMA protein-PHA combinations appeared to antagonize the suppression by dexamethasone .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4107 10.1443 1.0000 To be or not to be a responder in T-cell responses : proteinubiquitous oligopeptides in all proteins.
0.7251 0.9999 1.0000 To be or not to be a responder in cell_typeT-cell responses : ubiquitous oligopeptides in all proteins.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6098 10.1903 1.0000 Amino acid sequences of all proteinproteins are essays written in the same language.
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.8876 1.0000 1.0000 Accordingly, the same set of words and phrases ( oligopeptides ) appear in totally unrelated proteinproteins .
0.8286 1.0000 1.0000 Accordingly, the same set of words and phrases ( proteinoligopeptides ) appear in totally unrelated proteins .
Accordingly, the same set of words and phrases ( oligopeptides ) appear in totally proteinunrelated proteins .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6809 10.6959 1.0000 The reason that only certain individuals of particular major histocompatibility complex (MHC) haplotypes can mount T-cell responses against a given antigen of pathogens is found in the fact that proteinT-cell receptors are designed to recognize 18-20 residue-long peptide fragments sandwiched between two alpha-helices of class I or class II MHC molecules .
0.9150 1.0000 1.0000 The reason that only certain individuals of particular major histocompatibility complex (MHC) haplotypes can mount T-cell responses against a given antigen of pathogens is found in the fact that T-cell receptors are designed to recognize 18-20 residue-long peptide fragments sandwiched between two proteinalpha-helices of class I or class II MHC molecules .
3.6313 20.7671 10.7471 The reason that only certain individuals of particular proteinmajor histocompatibility complex (MHC) haplotypes can mount T-cell responses against a given antigen of pathogens is found in the fact that T-cell receptors are designed to recognize 18-20 residue-long peptide fragments sandwiched between two alpha-helices of class I or class II MHC molecules .
The reason that only certain individuals of particular major histocompatibility complex (MHC) haplotypes can mount T-cell responses against a given antigen of pathogens is found in the fact that T-cell receptors are designed to recognize 18-20 residue-long peptide fragments sandwiched between two alpha-helices of proteinclass I or class II MHC molecules .
The reason that only certain individuals of particular major histocompatibility complex (MHC) haplotypes can mount T-cell responses against a given antigen of pathogens is found in the fact that T-cell receptors are designed to recognize 18-20 residue-long peptide fragments sandwiched between two alpha-helices of class I or proteinclass II MHC molecules .
The reason that only certain individuals of particular proteinmajor histocompatibility complex (MHC) haplotypes can mount T-cell responses against a given antigen of pathogens is found in the fact that T-cell receptors are designed to recognize 18-20 residue-long peptide fragments sandwiched between two alpha-helices of class I or class II MHC molecules .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3310 20.4092 1.0000 Two distinct signal transmission pathways in cell_typeT lymphocytes are inhibited by complexes formed between an immunophilin and either FK506 or rapamycin .
1.6165 10.7080 1.0000 Two distinct signal transmission pathways in T lymphocytes are inhibited by complexes formed between an proteinimmunophilin and either FK506 or rapamycin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4845 20.0972 1.0000 Proliferation and immunologic function of T lymphocytes are initiated by signals from the proteinantigen receptor that are inhibited by the immunosuppressant FK506 but not by its structural analog, rapamycin .
2.4581 20.2467 1.0000 Proliferation and immunologic function of cell_typeT lymphocytes are initiated by signals from the antigen receptor that are inhibited by the immunosuppressant FK506 but not by its structural analog, rapamycin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2953 20.6916 1.0000 On the other hand, proteininterleukin 2 ( IL-2 )-induced signals are blocked by rapamycin but not by FK506 .
0.9763 1.0000 1.0000 On the other hand, interleukin 2 ( proteinIL-2 )-induced signals are blocked by rapamycin but not by FK506 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8803 20.8476 10.6262 Remarkably, these two drugs inhibit each other's actions, raising the possibility that both act by means of a common immunophilin ( proteinimmunosuppressant binding protein ).
0.8458 0.9997 1.0000 Remarkably, these two drugs inhibit each other's actions, raising the possibility that both act by means of a common proteinimmunophilin ( immunosuppressant binding protein ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7450 30.0733 10.7545 We find that the dissociation constant of rapamycin to the proteinFK506 binding protein FKBP (Kd = 0.2 nM) is close to the dissociation constant of FK506 to FKBP (Kd = 0.4 nM) and to their effective biologic inhibitory concentrations .
1.6496 10.6870 1.0000 We find that the dissociation constant of rapamycin to the FK506 binding protein FKBP (Kd = 0.2 nM) is close to the dissociation constant of FK506 to proteinFKBP (Kd = 0.4 nM) and to their effective biologic inhibitory concentrations .
0.9755 1.0000 1.0000 We find that the dissociation constant of rapamycin to the FK506 binding protein proteinFKBP (Kd = 0.2 nM) is close to the dissociation constant of FK506 to FKBP (Kd = 0.4 nM) and to their effective biologic inhibitory concentrations .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8949 20.2400 10.4106 However, an excess of rapamycin is needed to revert FK506 -mediated inhibition of IL-2 production , apoptosis , and transcriptional activation of NF-AT , a proteinT-cell-specific transcription factor necessary for IL-2 gene activation .
2.0983 20.3563 0.9894 However, an excess of rapamycin is needed to revert FK506 -mediated inhibition of IL-2 production , apoptosis , and transcriptional activation of NF-AT , a T-cell-specific transcription factor necessary for proteinIL-2 gene activation .
2.0889 20.4004 0.9998 However, an excess of rapamycin is needed to revert FK506 -mediated inhibition of IL-2 production , apoptosis , and transcriptional activation of NF-AT , a T-cell-specific transcription factor necessary for DNAIL-2 gene activation .
1.6644 10.2385 1.0000 However, an excess of rapamycin is needed to revert FK506 -mediated inhibition of IL-2 production , apoptosis , and transcriptional activation of proteinNF-AT , a T-cell-specific transcription factor necessary for IL-2 gene activation .
1.6103 10.2099 1.0000 However, an excess of rapamycin is needed to revert FK506 -mediated inhibition of proteinIL-2 production , apoptosis , and transcriptional activation of NF-AT , a T-cell-specific transcription factor necessary for IL-2 gene activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7475 10.1391 1.0000 Similarly, an excess of FK506 is needed to revert rapamycin -mediated inhibition of proteinIL-2 -induced proliferation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4318 20.5340 1.0000 The drug concentrations required for antagonism may be explained by the relative affinity of the drugs to, and by the abundance of, the proteinimmunophilin FKBP .
The drug concentrations required for antagonism may be explained by the relative affinity of the drugs to, and by the abundance of, the immunophilin proteinFKBP .
The drug concentrations required for antagonism may be explained by the relative affinity of the drugs to, and by the abundance of, the proteinimmunophilin FKBP .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7735 10.6130 1.0000 FKBP has been shown to catalyze the interconversion of the cis- and trans- rotamers of the peptidyl-prolyl amide bond of peptide substrates ; here we show that rapamycin , like FK506 , is a potent inhibitor of the rotamase activity of proteinFKBP (Ki = 0.2 nM).
0.9880 1.0000 1.0000 proteinFKBP has been shown to catalyze the interconversion of the cis- and trans- rotamers of the peptidyl-prolyl amide bond of peptide substrates ; here we show that rapamycin , like FK506 , is a potent inhibitor of the rotamase activity of FKBP (Ki = 0.2 nM).
0.8992 0.9999 1.0000 FKBP has been shown to catalyze the interconversion of the cis- and trans- rotamers of the peptidyl-prolyl amide bond of peptide substrates ; here we show that rapamycin , like FK506 , is a potent inhibitor of the proteinrotamase activity of FKBP (Ki = 0.2 nM).
FKBP has been shown to catalyze the interconversion of the cis- and trans- rotamers of the proteinpeptidyl-prolyl amide bond of peptide substrates ; here we show that rapamycin , like FK506 , is a potent inhibitor of the rotamase activity of FKBP (Ki = 0.2 nM).
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9463 1.0000 1.0000 Neither proteinFKBP binding nor inhibition of rotamase activity of FKBP alone is sufficient to explain the biologic actions of these drugs.
0.8993 1.0000 1.0000 Neither FKBP binding nor inhibition of rotamase activity of proteinFKBP alone is sufficient to explain the biologic actions of these drugs.
0.8186 1.0000 1.0000 Neither FKBP binding nor inhibition of proteinrotamase activity of FKBP alone is sufficient to explain the biologic actions of these drugs.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6915 10.3165 1.0000 Rather, these findings suggest that proteinimmunophilin bound to FK506 interferes with antigen receptor -induced signals , while rapamycin bound to the immunophilin interferes with IL-2 -induced signals .
1.6815 10.2855 1.0000 Rather, these findings suggest that immunophilin bound to FK506 interferes with antigen receptor -induced signals , while rapamycin bound to the proteinimmunophilin interferes with IL-2 -induced signals .
1.6110 10.5649 1.0000 Rather, these findings suggest that immunophilin bound to FK506 interferes with proteinantigen receptor -induced signals , while rapamycin bound to the immunophilin interferes with IL-2 -induced signals .
0.8973 1.0000 1.0000 Rather, these findings suggest that immunophilin bound to FK506 interferes with antigen receptor -induced signals , while rapamycin bound to the immunophilin interferes with proteinIL-2 -induced signals .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5496 20.3232 10.6963 Adherence-dependent increase in RNAhuman monocyte PDGF(B) mRNA is associated with increases in c-fos , c-jun , and EGR2 mRNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2483 20.6269 0.9993 Adherence is an important initial step in the transition of a circulating monocyte to a cell_typetissue macrophage .
2.1709 20.9283 0.9999 Adherence is an important initial step in the transition of a cell_typecirculating monocyte to a tissue macrophage .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5782 10.7172 1.0000 This differentiation is accompanied by an augmented capacity to generate proteingrowth factors .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.6306 30.0021 10.7297 We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased mRNA encoding profibrotic growth factors such as proteinplatelet-derived growth factor B subunit ( PDGF[B] ) and transforming growth factor-beta ( TGF-beta ).
3.5415 20.9986 10.7835 We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased mRNA encoding profibrotic growth factors such as platelet-derived growth factor B subunit ( PDGF[B] ) and proteintransforming growth factor-beta ( TGF-beta ).
1.6626 10.7205 1.0000 We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased RNAmRNA encoding profibrotic growth factors such as platelet-derived growth factor B subunit ( PDGF[B] ) and transforming growth factor-beta ( TGF-beta ).
0.9547 1.0000 1.0000 We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased mRNA encoding profibrotic growth factors such as platelet-derived growth factor B subunit ( PDGF[B] ) and transforming growth factor-beta ( proteinTGF-beta ).
0.7742 1.0000 1.0000 We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased mRNA encoding profibrotic growth factors such as platelet-derived growth factor B subunit ( proteinPDGF[B] ) and transforming growth factor-beta ( TGF-beta ).
2.1929 10.8162 10.3783 We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased mRNA encoding proteinprofibrotic growth factors such as platelet-derived growth factor B subunit ( PDGF[B] ) and transforming growth factor-beta ( TGF-beta ).
We hypothesized that adherence itself might be an important trigger for a sequence of gene activation culminating in cells with increased mRNA encoding profibrotic proteingrowth factors such as platelet-derived growth factor B subunit ( PDGF[B] ) and transforming growth factor-beta ( TGF-beta ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7899 10.9652 1.0000 After in vitro adherence, human monocytes had a biphasic increase in RNAPDGF(B) mRNA with peaks at 6 h and 13 d.
1.3754 10.8893 0.9930 After in vitro adherence, human monocytes had a biphasic increase in proteinPDGF(B) mRNA with peaks at 6 h and 13 d.
1.5810 10.8389 0.9999 After in vitro adherence, cell_typehuman monocytes had a biphasic increase in PDGF(B) mRNA with peaks at 6 h and 13 d.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7119 10.1964 1.0000 No increase in RNATGF-beta mRNA was observed.
1.2753 10.1340 0.9946 No increase in proteinTGF-beta mRNA was observed.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6767 20.2137 1.0000 The 6-h increase in RNAPDGF(B) mRNA was adherence dependent, and in addition, was abrogated when the cytoskeletal integrity was compromised by cytochalasin D .
2.3108 20.3890 0.9955 The 6-h increase in proteinPDGF(B) mRNA was adherence dependent, and in addition, was abrogated when the cytoskeletal integrity was compromised by cytochalasin D .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6604 20.0287 1.0000 The 6-h increase in RNAPDGF(B) mRNA was unaltered by adherence in the presence of the monocyte stimulus lipopolysaccharide .
2.1823 20.1433 0.9952 The 6-h increase in proteinPDGF(B) mRNA was unaltered by adherence in the presence of the monocyte stimulus lipopolysaccharide .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5729 20.4463 1.0000 Adherence to either fibronectin or collagen-coated plastic had little consistent effect on RNAPDGF(B) mRNA accumulation .
1.9814 20.3677 0.9885 Adherence to either fibronectin or collagen-coated plastic had little consistent effect on proteinPDGF(B) mRNA accumulation .
1.5783 10.5642 1.0000 Adherence to either proteinfibronectin or collagen-coated plastic had little consistent effect on PDGF(B) mRNA accumulation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5132 20.5569 10.9786 The increased PDGF(B) mRNA observed in adherent monocytes was accompanied by increases in mRNAs of the DNAearly growth response genes c-fos (maximal at 20 min), c-jun, and EGR2 (maximal at 6-24 h).
2.3664 20.3284 1.0000 The increased RNAPDGF(B) mRNA observed in adherent monocytes was accompanied by increases in mRNAs of the early growth response genes c-fos (maximal at 20 min), c-jun, and EGR2 (maximal at 6-24 h).
1.7350 20.4372 0.9858 The increased proteinPDGF(B) mRNA observed in adherent monocytes was accompanied by increases in mRNAs of the early growth response genes c-fos (maximal at 20 min), c-jun, and EGR2 (maximal at 6-24 h).
1.6775 10.6669 1.0000 The increased PDGF(B) mRNA observed in adherent monocytes was accompanied by increases in RNAmRNAs of the early growth response genes c-fos (maximal at 20 min), c-jun, and EGR2 (maximal at 6-24 h).
1.2678 10.4672 0.9999 The increased PDGF(B) mRNA observed in cell_typeadherent monocytes was accompanied by increases in mRNAs of the early growth response genes c-fos (maximal at 20 min), c-jun, and EGR2 (maximal at 6-24 h).
0.9482 1.0000 1.0000 The increased PDGF(B) mRNA observed in adherent monocytes was accompanied by increases in mRNAs of the early growth response genes DNAc-fos (maximal at 20 min), c-jun, and EGR2 (maximal at 6-24 h).
0.9099 1.0000 1.0000 The increased PDGF(B) mRNA observed in adherent monocytes was accompanied by increases in mRNAs of the early growth response genes c-fos (maximal at 20 min), c-jun, and DNAEGR2 (maximal at 6-24 h).
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4791 10.3918 0.9998 The increase in c-jun and EGR2, but not DNAc-fos , mRNA was also abrogated by cytochalasin D .
1.1828 10.2956 0.9998 The increase in c-jun and EGR2, but not RNAc-fos , mRNA was also abrogated by cytochalasin D .
0.5328 1.0000 0.9999 The increase in DNAc-jun and EGR2, but not c-fos , mRNA was also abrogated by cytochalasin D .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6066 10.4936 0.9998 These observations suggest that adherence results in increases of c-fos , c-jun , EGR2 , and RNAPDGF(B) mRNA .
1.0542 10.2047 1.0000 These observations suggest that adherence results in increases of RNAc-fos , c-jun , EGR2 , and PDGF(B) mRNA .
0.7476 1.0000 1.0000 These observations suggest that adherence results in increases of c-fos , c-jun , proteinEGR2 , and PDGF(B) mRNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6442 10.6969 1.0000 In addition, the increases in c-jun , EGR2 , and proteinPDGF(B) may depend on cytoskeletal rearrangement .
1.3837 10.6458 1.0000 In addition, the increases in DNAc-jun , EGR2 , and PDGF(B) may depend on cytoskeletal rearrangement .
0.9030 1.0000 1.0000 In addition, the increases in c-jun , proteinEGR2 , and PDGF(B) may depend on cytoskeletal rearrangement .
In addition, the increases in c-jun , DNAEGR2 , and PDGF(B) may depend on cytoskeletal rearrangement .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7571 20.8481 10.2515 Single cell assay of a transcription factor reveals a threshold in transcription activated by signals emanating from the proteinT-cell antigen receptor .
2.2485 20.7155 1.0000 Single cell assay of a proteintranscription factor reveals a threshold in transcription activated by signals emanating from the T-cell antigen receptor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2219 20.4764 1.0000 Stimulation of T lymphocytes through their antigen receptor leads to the appearance of several proteintranscription factors , including NF-AT and NF-kappa B , which are involved in regulating genes required for immunologic activation.
2.1676 20.1948 1.0000 Stimulation of T lymphocytes through their proteinantigen receptor leads to the appearance of several transcription factors , including NF-AT and NF-kappa B , which are involved in regulating genes required for immunologic activation.
2.1428 20.5654 0.9999 Stimulation of cell_typeT lymphocytes through their antigen receptor leads to the appearance of several transcription factors , including NF-AT and NF-kappa B , which are involved in regulating genes required for immunologic activation.
1.7411 10.3423 1.0000 Stimulation of T lymphocytes through their antigen receptor leads to the appearance of several transcription factors , including proteinNF-AT and NF-kappa B , which are involved in regulating genes required for immunologic activation.
1.5869 10.6612 1.0000 Stimulation of T lymphocytes through their antigen receptor leads to the appearance of several transcription factors , including NF-AT and proteinNF-kappa B , which are involved in regulating genes required for immunologic activation.
2.1800 20.7819 1.0000 Stimulation of T lymphocytes through their antigen receptor leads to the appearance of several transcription factors , including NF-AT and NF-kappa B , which are involved in DNAregulating genes required for immunologic activation.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6996 10.4535 1.0000 To investigate the activity of a single transcription factor in individual viable cells , we have applied an assay that uses the fluorescence-activated cell sorter to quantitate proteinbeta-galactosidase ( beta-gal ).
1.5856 10.8586 1.0000 To investigate the activity of a single proteintranscription factor in individual viable cells , we have applied an assay that uses the fluorescence-activated cell sorter to quantitate beta-galactosidase ( beta-gal ).
0.9658 1.0000 1.0000 To investigate the activity of a single transcription factor in individual viable cells , we have applied an assay that uses the fluorescence-activated cell sorter to quantitate beta-galactosidase ( proteinbeta-gal ).
To investigate the activity of a single transcription factor in cell_typeindividual viable cells , we have applied an assay that uses the fluorescence-activated cell sorter to quantitate beta-galactosidase ( beta-gal ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1553 30.1074 10.7825 We have analyzed the distribution of NF-AT transcriptional activity among T cells undergoing activation by using a construct in which three tandem copies of the DNANF-AT -binding site directs transcription of the lacZ gene .
2.2793 20.8444 0.9999 We have analyzed the distribution of NF-AT transcriptional activity among cell_typeT cells undergoing activation by using a construct in which three tandem copies of the NF-AT -binding site directs transcription of the lacZ gene .
2.2184 20.3718 0.9981 We have analyzed the distribution of NF-AT transcriptional activity among T cells undergoing activation by using a construct in which three tandem copies of the proteinNF-AT -binding site directs transcription of the lacZ gene .
2.1816 20.5223 0.9999 We have analyzed the distribution of NF-AT transcriptional activity among T cells undergoing activation by using a construct in which three tandem copies of the NF-AT -binding site directs transcription of the DNAlacZ gene .
1.5847 10.8117 1.0000 We have analyzed the distribution of proteinNF-AT transcriptional activity among T cells undergoing activation by using a construct in which three tandem copies of the NF-AT -binding site directs transcription of the lacZ gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7083 10.3799 1.0000 Unexpectedly, stimulation of cloned stably transfected Jurkat T cells leads to a bimodal pattern of beta-gal expression in which some cells express no proteinbeta-gal and others express high levels.
0.7538 0.9996 0.9987 Unexpectedly, stimulation of cloned stably transfected Jurkat cell_typeT cells leads to a bimodal pattern of beta-gal expression in which some cells express no beta-gal and others express high levels.
2.9863 10.8558 10.9475 Unexpectedly, stimulation of cloned stably transfected cell_lineJurkat T cells leads to a bimodal pattern of beta-gal expression in which some cells express no beta-gal and others express high levels.
0.8885 1.0000 1.0000 Unexpectedly, stimulation of cloned stably transfected Jurkat T cells leads to a bimodal pattern of proteinbeta-gal expression in which some cells express no beta-gal and others express high levels.
Unexpectedly, stimulation of cell_linecloned stably transfected Jurkat T cells leads to a bimodal pattern of beta-gal expression in which some cells express no beta-gal and others express high levels.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7382 10.3658 1.0000 Further results, in which beta-gal activity is correlated with NF-AT -binding activity , indicate that the concentration of proteinNF-AT must exceed a critical threshold before transcription initiates.
0.9374 1.0000 1.0000 Further results, in which proteinbeta-gal activity is correlated with NF-AT -binding activity , indicate that the concentration of NF-AT must exceed a critical threshold before transcription initiates.
0.9143 1.0000 1.0000 Further results, in which beta-gal activity is correlated with proteinNF-AT -binding activity , indicate that the concentration of NF-AT must exceed a critical threshold before transcription initiates.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7550 10.2657 1.0000 This threshold likely reflects the NF-AT concentration-dependent assembly of transcription complexes at the DNApromoter .
1.5295 10.9844 1.0000 This threshold likely reflects the NF-AT concentration-dependent assembly of proteintranscription complexes at the promoter .
0.9073 1.0000 1.0000 This threshold likely reflects the proteinNF-AT concentration-dependent assembly of transcription complexes at the promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3997 20.0983 1.0000 Similar constructs controlled by proteinNF-kappa B or the entire interleukin-2 enhancer show bimodal expression patterns during induction, suggesting that thresholds set by the concentration of transcription factors may be a common property of inducible genes .
2.3513 20.3182 1.0000 Similar constructs controlled by NF-kappa B or the entire DNAinterleukin-2 enhancer show bimodal expression patterns during induction, suggesting that thresholds set by the concentration of transcription factors may be a common property of inducible genes .
2.3270 20.5643 0.9999 Similar constructs controlled by NF-kappa B or the entire interleukin-2 enhancer show bimodal expression patterns during induction, suggesting that thresholds set by the concentration of transcription factors may be a common property of DNAinducible genes .
2.2899 20.4464 1.0000 Similar constructs controlled by NF-kappa B or the entire interleukin-2 enhancer show bimodal expression patterns during induction, suggesting that thresholds set by the concentration of proteintranscription factors may be a common property of inducible genes .
2.2430 20.1752 0.9905 Similar constructs controlled by NF-kappa B or the entire proteininterleukin-2 enhancer show bimodal expression patterns during induction, suggesting that thresholds set by the concentration of transcription factors may be a common property of inducible genes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3841 10.1196 30.1127 The DNAEpstein-Barr virus ( EBV ) BMRF1 promoter for early antigen ( EA-D ) is regulated by the EBV transactivators , BRLF1 and BZLF1 , in a cell-specific manner .
1.5488 10.7597 0.9999 The Epstein-Barr virus ( EBV ) BMRF1 promoter for proteinearly antigen ( EA-D ) is regulated by the EBV transactivators , BRLF1 and BZLF1 , in a cell-specific manner .
1.2658 20.6257 1.0000 The Epstein-Barr virus ( EBV ) BMRF1 promoter for early antigen ( EA-D ) is regulated by the proteinEBV transactivators , BRLF1 and BZLF1 , in a cell-specific manner .
0.9696 1.0000 1.0000 The Epstein-Barr virus ( EBV ) BMRF1 promoter for early antigen ( proteinEA-D ) is regulated by the EBV transactivators , BRLF1 and BZLF1 , in a cell-specific manner .
0.9624 1.0000 1.0000 The Epstein-Barr virus ( EBV ) BMRF1 promoter for early antigen ( EA-D ) is regulated by the EBV transactivators , BRLF1 and proteinBZLF1 , in a cell-specific manner .
0.9319 1.0000 1.0000 The Epstein-Barr virus ( EBV ) BMRF1 promoter for early antigen ( EA-D ) is regulated by the EBV transactivators , proteinBRLF1 and BZLF1 , in a cell-specific manner .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0299 10.1848 20.0972 The proteinEpstein-Barr virus early antigen diffuse component ( EA-D ) is essential for Epstein-Barr virus DNA polymerase activity , and its activity is suppressed during latent infection.
0.9567 1.0000 1.0000 The Epstein-Barr virus early antigen diffuse component ( proteinEA-D ) is essential for Epstein-Barr virus DNA polymerase activity , and its activity is suppressed during latent infection.
3.3634 30.2429 10.6559 The Epstein-Barr virus early antigen diffuse component ( EA-D ) is essential for proteinEpstein-Barr virus DNA polymerase activity , and its activity is suppressed during latent infection.
The Epstein-Barr virus early antigen diffuse component ( EA-D ) is essential for Epstein-Barr DNAvirus DNA polymerase activity , and its activity is suppressed during latent infection.
The Epstein-Barr virus proteinearly antigen diffuse component ( EA-D ) is essential for Epstein-Barr virus DNA polymerase activity , and its activity is suppressed during latent infection.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2717 20.9927 10.6313 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two proteinimmediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
2.0946 20.2764 0.9998 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in cell_typelymphoid cells and epithelial cells .
1.8000 10.1806 0.9999 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and proteinBRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
1.6686 10.1996 1.0000 We investigated the regulation of the DNApromoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
1.5385 10.8854 0.9995 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and cell_typeepithelial cells .
0.9506 1.0000 1.0000 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( proteinZ ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
0.9492 1.0000 1.0000 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( proteinR ), focusing on the differences in response in lymphoid cells and epithelial cells .
0.9397 1.0000 1.0000 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , proteinBZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
0.9196 1.0000 1.0000 We investigated the regulation of the promoter ( DNABMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
2.0316 20.7221 1.0000 We investigated the regulation of the promoter ( BMRF1 ) for this DNAearly gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
1.2958 10.6972 0.9998 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , BZLF1 ( Z ) and proteinBRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
1.1864 10.3820 0.9985 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , proteinBZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
0.5034 0.9926 1.0000 We investigated the regulation of the promoter ( BMRF1 ) for this early gene by studying its responsiveness in vitro to two immediate-early viral transactivators , proteinBZLF1 ( Z ) and BRLF1 ( R ), focusing on the differences in response in lymphoid cells and epithelial cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4336 20.8675 1.0000 In lymphoid cells , Z or R alone produced only small increases in DNAEA-D promoter activity , whereas both transactivators together produced a large stimulatory effect.
1.6422 10.2017 1.0000 In lymphoid cells , Z or R alone produced only small increases in EA-D promoter activity , whereas both proteintransactivators together produced a large stimulatory effect.
1.6083 10.7390 0.9998 In cell_typelymphoid cells , Z or R alone produced only small increases in EA-D promoter activity , whereas both transactivators together produced a large stimulatory effect.
0.9528 1.0000 1.0000 In lymphoid cells , Z or proteinR alone produced only small increases in EA-D promoter activity , whereas both transactivators together produced a large stimulatory effect.
0.9509 1.0000 1.0000 In lymphoid cells , proteinZ or R alone produced only small increases in EA-D promoter activity , whereas both transactivators together produced a large stimulatory effect.
In lymphoid cells , Z or R alone produced only small increases in proteinEA-D promoter activity , whereas both transactivators together produced a large stimulatory effect.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2227 20.5479 1.0000 In epithelial cells , the Z transactivator alone produced maximal stimulation of the DNAEA-D promoter ; the effect of R and Z together was no greater than that of Z alone.
2.2173 20.8333 1.0000 In epithelial cells , the Z transactivator alone produced maximal stimulation of the EA-D promoter ; the effect of R and Z together was no greater than that of proteinZ alone.
1.5936 10.6317 0.9998 In cell_typeepithelial cells , the Z transactivator alone produced maximal stimulation of the EA-D promoter ; the effect of R and Z together was no greater than that of Z alone.
1.4217 20.9014 0.9999 In epithelial cells , the proteinZ transactivator alone produced maximal stimulation of the EA-D promoter ; the effect of R and Z together was no greater than that of Z alone.
0.9421 1.0000 1.0000 In epithelial cells , the Z transactivator alone produced maximal stimulation of the EA-D promoter ; the effect of R and proteinZ together was no greater than that of Z alone.
0.8709 1.0000 1.0000 In epithelial cells , the Z transactivator alone produced maximal stimulation of the EA-D promoter ; the effect of proteinR and Z together was no greater than that of Z alone.
In epithelial cells , the Z transactivator alone produced maximal stimulation of the proteinEA-D promoter ; the effect of R and Z together was no greater than that of Z alone.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9483 20.1283 10.8938 Deletional analysis and site-directed mutagenesis of the EA-D promoter demonstrated that in epithelial cells the potential DNAAP-1 binding site plays an essential role in Z responsiveness, although sequences further upstream are also important.
2.2374 20.1238 1.0000 Deletional analysis and site-directed mutagenesis of the DNAEA-D promoter demonstrated that in epithelial cells the potential AP-1 binding site plays an essential role in Z responsiveness, although sequences further upstream are also important.
1.5394 10.9609 0.9999 Deletional analysis and site-directed mutagenesis of the EA-D promoter demonstrated that in cell_typeepithelial cells the potential AP-1 binding site plays an essential role in Z responsiveness, although sequences further upstream are also important.
0.9277 1.0000 1.0000 Deletional analysis and site-directed mutagenesis of the EA-D promoter demonstrated that in epithelial cells the potential AP-1 binding site plays an essential role in proteinZ responsiveness, although sequences further upstream are also important.
1.3998 10.5054 0.9962 Deletional analysis and site-directed mutagenesis of the EA-D promoter demonstrated that in epithelial cells the potential proteinAP-1 binding site plays an essential role in Z responsiveness, although sequences further upstream are also important.
Deletional analysis and site-directed mutagenesis of the proteinEA-D promoter demonstrated that in epithelial cells the potential AP-1 binding site plays an essential role in Z responsiveness, although sequences further upstream are also important.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2066 20.1719 0.9999 In lymphoid cells , only the DNAupstream sequences are required for transactivation by the Z/R combination, and the AP-1 site is dispensable.
1.6442 10.7976 0.9999 In cell_typelymphoid cells , only the upstream sequences are required for transactivation by the Z/R combination, and the AP-1 site is dispensable.
2.1956 20.2897 1.0000 In lymphoid cells , only the upstream sequences are required for transactivation by the Z/R combination, and the DNAAP-1 site is dispensable.
2.1162 20.1608 0.9884 In lymphoid cells , only the upstream sequences are required for transactivation by the Z/R combination, and the proteinAP-1 site is dispensable.
In lymphoid cells , only the upstream sequences are required for transactivation by the Z/R combination, and the proteinAP-1 site is dispensable.
In lymphoid cells , only the upstream sequences are required for transactivation by the proteinZ/R combination, and the AP-1 site is dispensable.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3428 30.8860 10.7619 These data suggest that DNAEA-D ( BMRF1 ) promoter regulation by Z and R is cell type specific and appears to involve different mechanisms in each cell type.
0.7664 1.0000 0.9945 These data suggest that EA-D ( proteinBMRF1 ) promoter regulation by Z and R is cell type specific and appears to involve different mechanisms in each cell type.
These data suggest that EA-D ( BMRF1 ) promoter regulation by Z and proteinR is cell type specific and appears to involve different mechanisms in each cell type.
These data suggest that EA-D ( DNABMRF1 ) promoter regulation by Z and R is cell type specific and appears to involve different mechanisms in each cell type.
These data suggest that proteinEA-D ( BMRF1 ) promoter regulation by Z and R is cell type specific and appears to involve different mechanisms in each cell type.
These data suggest that EA-D ( BMRF1 ) promoter regulation by proteinZ and R is cell type specific and appears to involve different mechanisms in each cell type.
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.8018 30.8944 20.5948 Complementary DNA encoding the proteinhuman T-cell FK506 -binding protein , a peptidylprolyl cis-trans isomerase distinct from cyclophilin .
3.9280 30.8778 10.8157 Complementary DNA encoding the human T-cell FK506 -binding protein , a proteinpeptidylprolyl cis-trans isomerase distinct from cyclophilin .
1.8916 20.1320 1.0000 Complementary DNA encoding the human T-cell FK506 -binding protein , a peptidylprolyl cis-trans isomerase distinct from proteincyclophilin .
0.7334 0.9982 0.9998 DNAComplementary DNA encoding the human T-cell FK506 -binding protein , a peptidylprolyl cis-trans isomerase distinct from cyclophilin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
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3.4941 20.7618 10.8462 After the recent discovery that the cyclosporin A -binding protein cyclophilin is identical to peptidylprolyl cis-trans isomerase , a proteincellular binding protein for FK506 was found to be distinct from cyclophilin but to have the same enzymatic activity .
3.1147 30.7224 0.9992 After the recent discovery that the proteincyclosporin A -binding protein cyclophilin is identical to peptidylprolyl cis-trans isomerase , a cellular binding protein for FK506 was found to be distinct from cyclophilin but to have the same enzymatic activity .
2.9328 20.8642 10.2168 After the recent discovery that the cyclosporin A -binding protein cyclophilin is identical to proteinpeptidylprolyl cis-trans isomerase , a cellular binding protein for FK506 was found to be distinct from cyclophilin but to have the same enzymatic activity .
1.5106 10.7764 1.0000 After the recent discovery that the cyclosporin A -binding protein cyclophilin is identical to peptidylprolyl cis-trans isomerase , a cellular binding protein for FK506 was found to be distinct from proteincyclophilin but to have the same enzymatic activity .
0.9680 0.9999 1.0000 After the recent discovery that the cyclosporin A -binding protein proteincyclophilin is identical to peptidylprolyl cis-trans isomerase , a cellular binding protein for FK506 was found to be distinct from cyclophilin but to have the same enzymatic activity .
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1.8233 20.7991 0.9999 In this study, we isolated a cDNA coding for FK506 -binding protein ( FKBP ) from human peripheral blood T cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for proteinbovine FKBP .
1.4358 10.4158 1.0000 In this study, we isolated a DNAcDNA coding for FK506 -binding protein ( FKBP ) from human peripheral blood T cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine FKBP .
0.9588 1.0000 1.0000 In this study, we isolated a cDNA coding for FK506 -binding protein ( proteinFKBP ) from human peripheral blood T cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine FKBP .
0.9167 1.0000 1.0000 In this study, we isolated a cDNA coding for FK506 -binding protein ( FKBP ) from human peripheral blood T cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine proteinFKBP .
4.8238 20.9625 10.9867 In this study, we isolated a cDNA coding for FK506 -binding protein ( FKBP ) from cell_typehuman peripheral blood T cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine FKBP .
4.2191 20.8993 10.7708 In this study, we isolated a cDNA coding for proteinFK506 -binding protein ( FKBP ) from human peripheral blood T cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine FKBP .
2.5806 20.2974 10.0503 In this study, we isolated a cDNA coding for FK506 -binding protein ( FKBP ) from human peripheral blood T cells by using mixed DNA20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine FKBP .
In this study, we isolated a cDNA coding for FK506 -binding protein ( FKBP ) from human peripheral blood cell_typeT cells by using mixed 20-mer oligonucleotide probes synthesized on the basis of the sequence, Glu-Asp-Gly-Lys-Lys-Phe-Asp , reported for bovine FKBP .
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2.9458 10.9819 10.9784 The DNA isolated contained an open reading frame encoding protein108 amino acid residues .
2.7606 10.7715 10.9432 The DNA isolated contained an DNAopen reading frame encoding 108 amino acid residues .
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4.4971 20.9679 10.5308 The first 40 residues of the deduced proteinamino acid sequence were identical to those of the reported amino-terminal sequence of bovine FKBP , indicating that the DNA sequence isolated represents the gene coding for FKBP .
1.7097 10.6121 1.0000 The first 40 residues of the deduced amino acid sequence were identical to those of the reported amino-terminal sequence of bovine FKBP , indicating that the DNA sequence isolated represents the gene coding for proteinFKBP .
0.9743 1.0000 1.0000 The first 40 residues of the deduced amino acid sequence were identical to those of the reported amino-terminal sequence of bovine proteinFKBP , indicating that the DNA sequence isolated represents the gene coding for FKBP .
2.2642 20.5161 1.0000 The first 40 residues of the deduced amino acid sequence were identical to those of the reported proteinamino-terminal sequence of bovine FKBP , indicating that the DNA sequence isolated represents the gene coding for FKBP .
1.4590 10.8283 0.9999 The first 40 residues of the deduced amino acid sequence were identical to those of the reported amino-terminal sequence of proteinbovine FKBP , indicating that the DNA sequence isolated represents the gene coding for FKBP .
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1.6321 10.3260 1.0000 Computer-assisted analysis of the deduced amino acid sequence indicates that FKBP exhibits no internal homology and does not have significant sequence similarity to any other amino acid sequences of known proteins, including proteincyclophilin .
1.6238 10.4440 1.0000 Computer-assisted analysis of the deduced amino acid sequence indicates that proteinFKBP exhibits no internal homology and does not have significant sequence similarity to any other amino acid sequences of known proteins, including cyclophilin .
3.8177 20.4776 10.7186 Computer-assisted analysis of the deduced proteinamino acid sequence indicates that FKBP exhibits no internal homology and does not have significant sequence similarity to any other amino acid sequences of known proteins, including cyclophilin .
3.7711 20.6907 10.8478 Computer-assisted analysis of the deduced amino acid sequence indicates that FKBP exhibits no internal homology and does not have significant sequence similarity to any other proteinamino acid sequences of known proteins, including cyclophilin .
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1.7328 10.0979 1.0000 This result suggests that two catalytically similar proteins, proteincyclophilin and FKBP , evolved independently.
0.9013 1.0000 1.0000 This result suggests that two catalytically similar proteins, cyclophilin and proteinFKBP , evolved independently.
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2.5258 20.2456 1.0000 In Northern blot analysis , RNAmRNA species of approximately 1.8 kilobases that hybridized with human FKBP cDNA were detected in poly(A)+ RNAs from brain , lung , liver , and placental cells and leukocytes .
2.4597 20.8137 0.9999 In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with DNAhuman FKBP cDNA were detected in poly(A)+ RNAs from brain , lung , liver , and placental cells and leukocytes .
2.3375 20.3489 1.0000 In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with human FKBP cDNA were detected in RNApoly(A)+ RNAs from brain , lung , liver , and placental cells and leukocytes .
1.4711 10.9792 0.9998 In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with human FKBP cDNA were detected in poly(A)+ RNAs from brain , lung , liver , and cell_typeplacental cells and leukocytes .
0.9482 1.0000 0.9941 In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with human proteinFKBP cDNA were detected in poly(A)+ RNAs from brain , lung , liver , and placental cells and leukocytes .
0.8212 1.0000 0.9999 In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with human FKBP cDNA were detected in poly(A)+ RNAs from brain , lung , liver , and placental cells and cell_typeleukocytes .
0.4568 0.9999 0.9999 In Northern blot analysis , mRNA species of approximately 1.8 kilobases that hybridized with human DNAFKBP cDNA were detected in poly(A)+ RNAs from brain , lung , liver , and placental cells and leukocytes .
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4.6928 20.3979 10.8603 Induction of cell_lineJurkat leukemic T cells with phorbol 12-myristate 13-acetate and ionomycin did not affect the level of FKBP mRNA .
2.2753 20.9400 1.0000 Induction of Jurkat leukemic T cells with phorbol 12-myristate 13-acetate and ionomycin did not affect the level of RNAFKBP mRNA .
1.7110 20.9350 0.9812 Induction of Jurkat leukemic T cells with phorbol 12-myristate 13-acetate and ionomycin did not affect the level of proteinFKBP mRNA .
Induction of Jurkat leukemic cell_typeT cells with phorbol 12-myristate 13-acetate and ionomycin did not affect the level of FKBP mRNA .
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1.6939 10.2824 1.0000 Southern blot analysis of human genomic DNA digested with different restriction enzymes suggests the existence of only a few copies of the DNA sequence encoding proteinFKBP .
1.2761 10.9713 0.9999 Southern blot analysis of human genomic DNA digested with different proteinrestriction enzymes suggests the existence of only a few copies of the DNA sequence encoding FKBP .
2.2803 20.9385 0.9999 Southern blot analysis of human genomic DNA digested with different restriction enzymes suggests the existence of only a few copies of the DNADNA sequence encoding FKBP .
1.2986 20.1150 0.9998 Southern blot analysis of human DNAgenomic DNA digested with different restriction enzymes suggests the existence of only a few copies of the DNA sequence encoding FKBP .
Southern blot analysis of DNAhuman genomic DNA digested with different restriction enzymes suggests the existence of only a few copies of the DNA sequence encoding FKBP .
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2.2851 20.1983 1.0000 This is in contrast to the result that as many as 20 copies of the DNAcyclophilin gene and possible pseudogenes may be present in the mammalian genome .
2.1306 20.2084 0.9890 This is in contrast to the result that as many as 20 copies of the proteincyclophilin gene and possible pseudogenes may be present in the mammalian genome .
1.5540 10.9059 0.9999 This is in contrast to the result that as many as 20 copies of the cyclophilin gene and possible pseudogenes may be present in the DNAmammalian genome .
1.7308 10.1298 1.0000 This is in contrast to the result that as many as 20 copies of the cyclophilin gene and possible DNApseudogenes may be present in the mammalian genome .
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3.4837 20.4364 10.6986 Involvement of a second DNAlymphoid-specific enhancer element in the regulation of immunoglobulin heavy-chain gene expression .
2.2395 20.8165 0.9999 Involvement of a second lymphoid-specific enhancer element in the regulation of DNAimmunoglobulin heavy-chain gene expression .
1.6218 20.6453 0.8427 Involvement of a second lymphoid-specific enhancer element in the regulation of proteinimmunoglobulin heavy-chain gene expression .
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4.8037 30.9015 10.9228 To determine whether enhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the DNAimmunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
1.9277 20.5681 0.9999 To determine whether enhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the DNAbinding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
1.8646 20.5717 0.9999 To determine whether DNAenhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
1.3938 0.9985 10.2259 To determine whether enhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the DNAmurine IgH enhancer .
0.9113 1.0000 1.0000 To determine whether enhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated proteinNF-microB , in the murine IgH enhancer .
6.1588 30.7886 20.2042 To determine whether enhancer elements in addition to the DNAhighly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
3.5827 30.3538 10.3207 To determine whether enhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional proteinlymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
To determine whether enhancer elements in addition to the highly conserved octamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a proteinputative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
To determine whether enhancer elements in addition to the highly conserved DNAoctamer (OCTA)-nucleotide motif are important for lymphoid-specific expression of the immunoglobulin heavy-chain (IgH) gene , we have investigated the effect of mutating the binding site for a putative additional lymphoid-specific transcription factor , designated NF-microB , in the murine IgH enhancer .
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2.2979 20.7130 1.0000 We demonstrate that the DNANF-microB-binding site plays a critical role in the IgH enhancer , because mutation of the microB DNA motif decreased transcriptional activity of the IgH enhancer in cells of the B-cell lineage but not in nonlymphoid cells .
2.1206 20.7085 0.9999 We demonstrate that the NF-microB-binding site plays a critical role in the DNAIgH enhancer , because mutation of the microB DNA motif decreased transcriptional activity of the IgH enhancer in cells of the B-cell lineage but not in nonlymphoid cells .
2.1101 20.3406 1.0000 We demonstrate that the NF-microB-binding site plays a critical role in the IgH enhancer , because mutation of the microB DNA motif decreased transcriptional activity of the DNAIgH enhancer in cells of the B-cell lineage but not in nonlymphoid cells .
1.4966 10.9615 0.9999 We demonstrate that the NF-microB-binding site plays a critical role in the IgH enhancer , because mutation of the microB DNA motif decreased transcriptional activity of the IgH enhancer in cells of the cell_typeB-cell lineage but not in nonlymphoid cells .
1.4547 10.8032 0.9997 We demonstrate that the NF-microB-binding site plays a critical role in the IgH enhancer , because mutation of the microB DNA motif decreased transcriptional activity of the IgH enhancer in cells of the B-cell lineage but not in cell_typenonlymphoid cells .
3.6098 20.7045 10.8074 We demonstrate that the NF-microB-binding site plays a critical role in the IgH enhancer , because mutation of the DNAmicroB DNA motif decreased transcriptional activity of the IgH enhancer in cells of the B-cell lineage but not in nonlymphoid cells .
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1.5841 10.6661 0.9999 This effect was comparable to or even stronger than the effect of a mutation in the DNAOCTA site .
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2.2394 20.3548 0.9998 Moreover, combined mutation of both microB and OCTA sites further reduced enhancer activity in cell_typelymphoid cells .
0.5940 0.9999 0.9997 Moreover, combined mutation of both DNAmicroB and OCTA sites further reduced enhancer activity in lymphoid cells .
0.6877 0.9996 0.9950 Moreover, combined mutation of both microB and DNAOCTA sites further reduced enhancer activity in lymphoid cells .
Moreover, combined mutation of both microB and DNAOCTA sites further reduced enhancer activity in lymphoid cells .
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2.3151 20.4751 0.9999 Interestingly, alteration of either the microB or E3 site in a DNA70-base-pair fragment of the IgH enhancer that lacks the binding site for OCTA abolished enhancer activity in lymphoid cells completely.
1.5237 10.8349 0.9999 Interestingly, alteration of either the microB or E3 site in a 70-base-pair fragment of the DNAIgH enhancer that lacks the binding site for OCTA abolished enhancer activity in lymphoid cells completely.
1.5061 10.8455 0.9997 Interestingly, alteration of either the microB or E3 site in a 70-base-pair fragment of the IgH enhancer that lacks the binding site for OCTA abolished enhancer activity in cell_typelymphoid cells completely.
1.5203 20.5256 0.9993 Interestingly, alteration of either the microB or E3 site in a 70-base-pair fragment of the IgH enhancer that lacks the DNAbinding site for OCTA abolished enhancer activity in lymphoid cells completely.
0.8822 0.9999 1.0000 Interestingly, alteration of either the microB or E3 site in a 70-base-pair fragment of the IgH enhancer that lacks the binding site for proteinOCTA abolished enhancer activity in lymphoid cells completely.
Interestingly, alteration of either the DNAmicroB or E3 site in a 70-base-pair fragment of the IgH enhancer that lacks the binding site for OCTA abolished enhancer activity in lymphoid cells completely.
Interestingly, alteration of either the microB or DNAE3 site in a 70-base-pair fragment of the IgH enhancer that lacks the binding site for OCTA abolished enhancer activity in lymphoid cells completely.
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2.3656 20.0020 1.0000 Nevertheless, a multimer of the DNAmicroB motif alone showed no enhancer activity .
Nevertheless, a multimer of the DNAmicroB motif alone showed no enhancer activity .
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3.0036 20.3530 10.5982 DNase footprinting analysis corroborated the functional data showing that a lymphoid-specific protein binds to the DNAmicroB DNA motif .
2.1630 20.2675 1.0000 DNase footprinting analysis corroborated the functional data showing that a proteinlymphoid-specific protein binds to the microB DNA motif .
0.9724 1.0000 1.0000 proteinDNase footprinting analysis corroborated the functional data showing that a lymphoid-specific protein binds to the microB DNA motif .
DNase footprinting analysis corroborated the functional data showing that a lymphoid-specific protein binds to the DNAmicroB DNA motif .
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2.3610 20.3149 1.0000 Our results suggest that the DNAmicroB element is a new crucial element important for lymphoid-specific expression of the IgH gene but that interaction with another enhancer element is essential for its activity.
2.2960 20.3109 1.0000 Our results suggest that the microB element is a new crucial element important for lymphoid-specific expression of the IgH gene but that interaction with another DNAenhancer element is essential for its activity.
1.6083 20.3189 0.9721 Our results suggest that the DNAmicroB element is a new crucial element important for lymphoid-specific expression of the IgH gene but that interaction with another enhancer element is essential for its activity.
2.3985 20.3150 1.0000 Our results suggest that the microB element is a new crucial element important for lymphoid-specific expression of the DNAIgH gene but that interaction with another enhancer element is essential for its activity.
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2.2577 30.0957 10.0951 Stimulation of the human immunodeficiency virus type 2 ( HIV-2 ) gene expression by the cytomegalovirus and DNAHIV-2 transactivator gene .
5.6278 20.8189 30.5220 Stimulation of the DNAhuman immunodeficiency virus type 2 ( HIV-2 ) gene expression by the cytomegalovirus and HIV-2 transactivator gene .
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2.4834 10.9467 10.5681 The DNAtransactivator (IE-2) gene of the human cytomegalovirus ( CMV ) can enhance HIV-2 as well as HIV-1 gene expression in vitro.
1.9876 20.4124 0.9998 The transactivator (IE-2) gene of the human cytomegalovirus ( CMV ) can enhance HIV-2 as well as DNAHIV-1 gene expression in vitro.
0.5957 1.0000 0.9930 The proteintransactivator (IE-2) gene of the human cytomegalovirus ( CMV ) can enhance HIV-2 as well as HIV-1 gene expression in vitro.
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3.7061 20.9067 10.7469 This inducer can act in concert with the HIV-2 tat gene and T-cell activation in enhancing gene expression in cell_typehuman CD4+ lymphocytes .
3.7012 20.6387 10.5519 This inducer can act in concert with the DNAHIV-2 tat gene and T-cell activation in enhancing gene expression in human CD4+ lymphocytes .
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1.5668 10.8879 0.9999 While the HIV-2 and HIV-1 tat genes and proteinT-cell activators apparently employ independent modes of action, the CMV transactivator in combination with the HIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components.
1.3041 10.9762 0.9999 While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action, the CMV transactivator in combination with the HIV-2 tat or proteinT-cell activators may employ a gene activation pathway with some common and some distinct components.
2.2844 20.8420 1.0000 While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action, the proteinCMV transactivator in combination with the HIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components.
1.3459 10.1573 0.9999 While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action, the CMV transactivator in combination with the proteinHIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components.
While the HIV-2 and DNAHIV-1 tat genes and T-cell activators apparently employ independent modes of action, the CMV transactivator in combination with the HIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components.
While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action, the CMV transactivator in combination with the DNAHIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components.
While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action, the DNACMV transactivator in combination with the HIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components.
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1.5817 10.8181 1.0000 Both HIV-2 and CMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with proteinCMV transactivator affecting elongation more than the initiation .
1.1248 10.2440 1.0000 Both HIV-2 and proteinCMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with CMV transactivator affecting elongation more than the initiation .
Both HIV-2 and CMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with DNACMV transactivator affecting elongation more than the initiation .
Both HIV-2 and CMV proteintransactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with CMV transactivator affecting elongation more than the initiation .
Both HIV-2 and DNACMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with CMV transactivator affecting elongation more than the initiation .
Both HIV-2 and CMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation , with CMV proteintransactivator affecting elongation more than the initiation .
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2.3526 20.0184 1.0000 A significant proportion of transcripts appear to terminate prematurely in the absence of proteintransactivators .
1.1845 10.6226 1.0000 A significant proportion of RNAtranscripts appear to terminate prematurely in the absence of transactivators .
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3.9464 20.7994 10.6033 Deletion mutation analysis of the DNAHIV-2 long terminal repeat ( LTR ) suggests that the element that responds to CMV transactivation in human CD4+ lymphocytes is either a diffuse one or located downstream of the HIV-2 enhancer element .
3.9378 30.0084 10.5616 Deletion mutation analysis of the HIV-2 long terminal repeat ( LTR ) suggests that the element that responds to CMV transactivation in human CD4+ lymphocytes is either a diffuse one or located downstream of the DNAHIV-2 enhancer element .
0.9396 1.0000 1.0000 Deletion mutation analysis of the HIV-2 long terminal repeat ( DNALTR ) suggests that the element that responds to CMV transactivation in human CD4+ lymphocytes is either a diffuse one or located downstream of the HIV-2 enhancer element .
3.8871 20.3141 10.8423 Deletion mutation analysis of the HIV-2 long terminal repeat ( LTR ) suggests that the element that responds to CMV transactivation in cell_linehuman CD4+ lymphocytes is either a diffuse one or located downstream of the HIV-2 enhancer element .
Deletion mutation analysis of the HIV-2 long terminal repeat ( LTR ) suggests that the element that responds to CMV transactivation in cell_typehuman CD4+ lymphocytes is either a diffuse one or located downstream of the HIV-2 enhancer element .
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1.5652 10.9919 1.0000 Quantitative immunohistochemical analysis of cell_typemononuclear infiltrates in breast carcinomas --correlation with tumour differentiation .
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3.9513 20.5433 10.7438 Inflammatory infiltrates were analysed in tissue sections of 76 breast carcinomas by counting the percentage of macrophages , IgA+ and IgG+ plasma cells , T cells with their subpopulations, and cell_typenatural killer cells , and by measuring postcapillary venules ( PCVs , found in 12 cases) within the infiltrates.
2.5306 20.9212 0.9999 Inflammatory infiltrates were analysed in tissue sections of 76 breast carcinomas by counting the percentage of macrophages , IgA+ and IgG+ plasma cells , cell_typeT cells with their subpopulations, and natural killer cells , and by measuring postcapillary venules ( PCVs , found in 12 cases) within the infiltrates.
0.9186 1.0000 1.0000 Inflammatory infiltrates were analysed in tissue sections of 76 breast carcinomas by counting the percentage of cell_typemacrophages , IgA+ and IgG+ plasma cells , T cells with their subpopulations, and natural killer cells , and by measuring postcapillary venules ( PCVs , found in 12 cases) within the infiltrates.
0.8147 0.9988 0.9999 cell_typeInflammatory infiltrates were analysed in tissue sections of 76 breast carcinomas by counting the percentage of macrophages , IgA+ and IgG+ plasma cells , T cells with their subpopulations, and natural killer cells , and by measuring postcapillary venules ( PCVs , found in 12 cases) within the infiltrates.
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1.7067 10.7742 1.0000 These parameters were correlated with nuclear grade and biochemically determined proteinhormone receptor status , known markers of tumour differentiation .
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2.4638 20.7881 1.0000 A direct correlation was found between the extent of inflammation and nuclear grade (P less than 0.0001), and an inverse correlation between inflammation and proteinoestrogen receptor ( OR ) positivity (P less than 0.05) as well as inflammation and progesterone receptor ( PR ) positivity (P less than 0.05).
2.4612 20.7878 1.0000 A direct correlation was found between the extent of inflammation and nuclear grade (P less than 0.0001), and an inverse correlation between inflammation and oestrogen receptor ( OR ) positivity (P less than 0.05) as well as inflammation and proteinprogesterone receptor ( PR ) positivity (P less than 0.05).
0.9813 1.0000 1.0000 A direct correlation was found between the extent of inflammation and nuclear grade (P less than 0.0001), and an inverse correlation between inflammation and oestrogen receptor ( OR ) positivity (P less than 0.05) as well as inflammation and progesterone receptor ( proteinPR ) positivity (P less than 0.05).
0.9704 1.0000 1.0000 A direct correlation was found between the extent of inflammation and nuclear grade (P less than 0.0001), and an inverse correlation between inflammation and oestrogen receptor ( proteinOR ) positivity (P less than 0.05) as well as inflammation and progesterone receptor ( PR ) positivity (P less than 0.05).
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5.5600 30.3298 10.7901 The percentage of the cell_typeOKT8+ suppressor/cytotoxic T cells increased when the inflammation expanded from scanty to moderate (P less than 0.02).
The percentage of the OKT8+ suppressor/cytotoxic cell_typeT cells increased when the inflammation expanded from scanty to moderate (P less than 0.02).
The percentage of the cell_lineOKT8+ suppressor/cytotoxic T cells increased when the inflammation expanded from scanty to moderate (P less than 0.02).
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1.3194 10.1553 1.0000 The diameter of the DNAPCVs also increased with increasing inflammatory infiltrate (P less than 0.02).
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4.0972 30.2830 10.4171 In addition, a direct correlation exists between the diameter of the PCVs and both the percentage of the OKT8+ T cells (P less than 0.04) and the cell_typeLeu-7+ natural killer cells (P less than 0.03).
3.8517 30.3863 10.7185 In addition, a direct correlation exists between the diameter of the PCVs and both the percentage of the cell_typeOKT8+ T cells (P less than 0.04) and the Leu-7+ natural killer cells (P less than 0.03).
1.4941 10.4375 1.0000 In addition, a direct correlation exists between the diameter of the DNAPCVs and both the percentage of the OKT8+ T cells (P less than 0.04) and the Leu-7+ natural killer cells (P less than 0.03).
In addition, a direct correlation exists between the diameter of the PCVs and both the percentage of the cell_lineOKT8+ T cells (P less than 0.04) and the Leu-7+ natural killer cells (P less than 0.03).
In addition, a direct correlation exists between the diameter of the PCVs and both the percentage of the OKT8+ cell_typeT cells (P less than 0.04) and the Leu-7+ natural killer cells (P less than 0.03).
In addition, a direct correlation exists between the diameter of the PCVs and both the percentage of the OKT8+ T cells (P less than 0.04) and the Leu-7+ cell_typenatural killer cells (P less than 0.03).
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3.5141 20.2463 10.5917 Reactivity of lymphocytes to a proteinprogesterone receptor-specific monoclonal antibody .
1.3929 10.9587 1.0000 Reactivity of cell_typelymphocytes to a progesterone receptor-specific monoclonal antibody .
Reactivity of cell_linelymphocytes to a progesterone receptor-specific monoclonal antibody .
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4.3770 20.6803 10.8064 In this study we present evidence for reactivity of pregnancy lymphocytes , but not nonpregnancy lymphocytes , with the proteinprogesterone receptor-specific monoclonal antibody mPRI .
1.9848 20.2415 0.9998 In this study we present evidence for reactivity of pregnancy lymphocytes , but not cell_typenonpregnancy lymphocytes , with the progesterone receptor-specific monoclonal antibody mPRI .
1.9791 20.5400 0.9999 In this study we present evidence for reactivity of cell_typepregnancy lymphocytes , but not nonpregnancy lymphocytes , with the progesterone receptor-specific monoclonal antibody mPRI .
0.9685 0.9999 1.0000 In this study we present evidence for reactivity of pregnancy lymphocytes , but not nonpregnancy lymphocytes , with the progesterone receptor-specific monoclonal antibody proteinmPRI .
In this study we present evidence for reactivity of pregnancy lymphocytes , but not nonpregnancy cell_linelymphocytes , with the progesterone receptor-specific monoclonal antibody mPRI .
In this study we present evidence for reactivity of pregnancy cell_linelymphocytes , but not nonpregnancy lymphocytes , with the progesterone receptor-specific monoclonal antibody mPRI .
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2.4383 20.8174 1.0000 Using an avidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of pregnancy lymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of cell_typenonpregnancy lymphocytes reacted with the antibody.
2.4047 20.5079 1.0000 Using an avidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of cell_typepregnancy lymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of nonpregnancy lymphocytes reacted with the antibody.
1.7478 10.0317 0.9999 Using an proteinavidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of pregnancy lymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of nonpregnancy lymphocytes reacted with the antibody.
0.6870 0.9999 0.9997 Using an avidin protein-biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of pregnancy lymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of nonpregnancy lymphocytes reacted with the antibody.
1.9930 20.2803 0.9997 Using an proteinavidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of pregnancy lymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of nonpregnancy lymphocytes reacted with the antibody.
Using an avidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of pregnancy lymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of nonpregnancy cell_linelymphocytes reacted with the antibody.
Using an avidin -biotin peroxidase detection system , we found a nuclear staining in 14.6 +/- 3.7% (mean +/- SEM, N = 27) of pregnancy cell_linelymphocytes , while only 0.47 +/- 0.33% (mean +/- SEM, N = 15) of nonpregnancy lymphocytes reacted with the antibody.
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1.6085 20.4195 0.9376 Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of proteinprogesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
3.6964 20.4889 10.6355 Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of cell_typeprogesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
2.7487 20.3451 10.8311 Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of progesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of cell_typepositively staining lymphocytes .
2.2364 20.5681 0.9999 Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of progesterone receptor -bearing cells , while depletion of cell_typeCD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
2.2309 20.4864 0.9999 Depletion of cell_typeCD8+ cells was accompanied by 62 +/- 18% loss of progesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of progesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining cell_linelymphocytes .
Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of cell_lineprogesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
Depletion of CD8+ cells was accompanied by 62 +/- 18% loss of progesterone receptor -bearing cells , while depletion of cell_lineCD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
Depletion of cell_lineCD8+ cells was accompanied by 62 +/- 18% loss of progesterone receptor -bearing cells , while depletion of CD4+ cells resulted in a twofold increase in the number of positively staining lymphocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3549 20.8375 0.9999 In nonpregnancy lymphocytes a 3-day PHA treatment , as well as allogeneic stimulation, resulted in a significant increase in the number of cell_typereceptor-containing cells .
1.8469 10.1162 1.0000 In nonpregnancy lymphocytes a 3-day proteinPHA treatment , as well as allogeneic stimulation, resulted in a significant increase in the number of receptor-containing cells .
1.5574 10.8659 0.9998 In cell_typenonpregnancy lymphocytes a 3-day PHA treatment , as well as allogeneic stimulation, resulted in a significant increase in the number of receptor-containing cells .
In cell_linenonpregnancy lymphocytes a 3-day PHA treatment , as well as allogeneic stimulation, resulted in a significant increase in the number of receptor-containing cells .
In nonpregnancy cell_linelymphocytes a 3-day PHA treatment , as well as allogeneic stimulation, resulted in a significant increase in the number of receptor-containing cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2501 10.9560 10.8856 These results suggest that pregnancy , but not nonpregnancy , lymphocytes contain proteinprogesterone binding structures , and that these are inducible by mitogenic or alloantigenic stimuli .
0.9239 1.0000 1.0000 These results suggest that pregnancy , but not nonpregnancy , cell_typelymphocytes contain progesterone binding structures , and that these are inducible by mitogenic or alloantigenic stimuli .
These results suggest that pregnancy , but not nonpregnancy , cell_linelymphocytes contain progesterone binding structures , and that these are inducible by mitogenic or alloantigenic stimuli .
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2.8637 10.9698 10.5979 Activation of cell_typehuman CD4 T lymphocytes .
Activation of cell_linehuman CD4 T lymphocytes .
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1.3914 10.0033 1.0000 Interaction of fibronectin with proteinVLA-5 receptor on CD4 cells induces the AP-1 transcription factor .
1.3648 10.5670 1.0000 Interaction of proteinfibronectin with VLA-5 receptor on CD4 cells induces the AP-1 transcription factor .
1.0206 10.5766 0.9995 Interaction of fibronectin with VLA-5 receptor on CD4 cells induces the proteinAP-1 transcription factor .
1.3720 10.6258 0.9998 Interaction of fibronectin with VLA-5 receptor on cell_typeCD4 cells induces the AP-1 transcription factor .
1.2869 10.8573 0.9991 Interaction of fibronectin with VLA-5 receptor on CD4 cells induces the proteinAP-1 transcription factor .
Interaction of fibronectin with VLA-5 receptor on cell_lineCD4 cells induces the AP-1 transcription factor .
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1.7470 10.0697 1.0000 Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with proteinanti-CD3 alone or fibronectin alone.
1.5551 10.2849 1.0000 Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or proteinfibronectin alone.
1.4973 10.7417 1.0000 Fibronectin synergized with proteinanti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone.
0.9689 1.0000 1.0000 proteinFibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone.
1.4755 10.9547 0.9999 Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when cell_typeCD4 cells were cultured with anti-CD3 alone or fibronectin alone.
1.4680 10.8289 0.9999 Fibronectin synergized with anti-CD3 antibody to promote cell_typeCD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone.
Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when cell_lineCD4 cells were cultured with anti-CD3 alone or fibronectin alone.
Fibronectin synergized with anti-CD3 antibody to promote proteinCD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone.
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2.8316 10.9949 10.9289 In addition, anti-CD29 ( proteinintegrin beta 1 ) as well as anti-VLA-5 ( human fibronectin receptor ) antibodies blocked this CD4 cell activation in this system.
1.5514 10.6655 1.0000 In addition, proteinanti-CD29 ( integrin beta 1 ) as well as anti-VLA-5 ( human fibronectin receptor ) antibodies blocked this CD4 cell activation in this system.
0.8321 1.0000 0.9237 In addition, anti-CD29 ( integrin beta 1 ) as well as anti-VLA-5 ( proteinhuman fibronectin receptor ) antibodies blocked this CD4 cell activation in this system.
3.3980 20.8673 10.9198 In addition, anti-CD29 ( integrin beta 1 ) as well as proteinanti-VLA-5 ( human fibronectin receptor ) antibodies blocked this CD4 cell activation in this system.
In addition, anti-CD29 ( integrin beta 1 ) as well as anti-VLA-5 ( human proteinfibronectin receptor ) antibodies blocked this CD4 cell activation in this system.
In addition, anti-CD29 ( integrin beta 1 ) as well as proteinanti-VLA-5 ( human fibronectin receptor ) antibodies blocked this CD4 cell activation in this system.
In addition, anti-CD29 ( integrin beta 1 ) as well as anti-VLA-5 ( human fibronectin receptor ) antibodies blocked this cell_lineCD4 cell activation in this system.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6441 10.0361 1.0000 Although anti-CD3 alone or proteinfibronectin alone cannot induce IL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells .
1.5554 10.3154 1.0000 Although anti-CD3 alone or fibronectin alone cannot induce proteinIL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells .
1.5246 10.8340 1.0000 Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells , the combination of proteinanti-CD3 plus fibronectin induced IL-2 message by CD4 cells .
0.9209 0.9999 1.0000 Although proteinanti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells .
0.8856 1.0000 1.0000 Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells , the combination of anti-CD3 plus proteinfibronectin induced IL-2 message by CD4 cells .
0.8569 1.0000 1.0000 Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced proteinIL-2 message by CD4 cells .
1.4382 10.7543 0.9999 Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by cell_typeCD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells .
1.4032 10.6096 0.9998 Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by cell_typeCD4 cells .
Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by cell_lineCD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells .
Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells , the combination of anti-CD3 plus fibronectin induced IL-2 message by cell_lineCD4 cells .
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3.7194 20.8034 10.5816 In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a fibronectin -VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an proteinAP-1 transcriptional factor .
1.6549 10.2527 1.0000 In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a fibronectin -VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the proteinCD3 pathway of activation by the induction of an AP-1 transcriptional factor .
1.6021 10.4501 0.9982 In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a proteinfibronectin -VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor .
1.5326 10.5802 1.0000 In an analysis of the molecular mechanism by which proteinIL-2 message was generated, we showed that a fibronectin -VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor .
0.9710 1.0000 0.9859 In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a fibronectin -VLA-5 proteinfibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor .
0.8959 0.9988 1.0000 In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a fibronectin -VLA-5 proteinfibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor .
2.0332 20.7111 0.9998 In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a proteinfibronectin -VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6481 20.2944 10.2472 Thus the proteinVLA-5 fibronectin receptor on CD4 cells can play a complementary role in CD3 - TCR -mediated signal transduction through its interaction with fibronectin .
1.4783 10.3906 1.0000 Thus the VLA-5 fibronectin receptor on CD4 cells can play a complementary role in CD3 - TCR -mediated signal transduction through its interaction with proteinfibronectin .
0.9749 1.0000 1.0000 Thus the VLA-5 fibronectin receptor on CD4 cells can play a complementary role in CD3 - proteinTCR -mediated signal transduction through its interaction with fibronectin .
0.9064 1.0000 0.9713 Thus the VLA-5 proteinfibronectin receptor on CD4 cells can play a complementary role in CD3 - TCR -mediated signal transduction through its interaction with fibronectin .
0.8838 0.9996 1.0000 Thus the VLA-5 fibronectin receptor on CD4 cells can play a complementary role in proteinCD3 - TCR -mediated signal transduction through its interaction with fibronectin .
1.4515 10.7955 0.9996 Thus the VLA-5 fibronectin receptor on cell_typeCD4 cells can play a complementary role in CD3 - TCR -mediated signal transduction through its interaction with fibronectin .
Thus the VLA-5 fibronectin receptor on cell_lineCD4 cells can play a complementary role in CD3 - TCR -mediated signal transduction through its interaction with fibronectin .
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1.4732 10.8455 0.9999 Glucocorticoid receptors on cell_typemononuclear leukocytes in Alzheimer's disease .
0.8580 0.9992 1.0000 proteinGlucocorticoid receptors on mononuclear leukocytes in Alzheimer's disease .
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2.3684 20.2330 1.0000 In an exploration of the potential role of the glucocorticoid receptor (GR) in AD , GR density and affinity were assessed on cell_typemononuclear leukocytes of 12 AD patients and 12 healthy controls .
2.3184 20.7241 1.0000 In an exploration of the potential role of the proteinglucocorticoid receptor (GR) in AD , GR density and affinity were assessed on mononuclear leukocytes of 12 AD patients and 12 healthy controls .
0.9589 1.0000 1.0000 In an exploration of the potential role of the glucocorticoid receptor (GR) in AD , proteinGR density and affinity were assessed on mononuclear leukocytes of 12 AD patients and 12 healthy controls .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9909 1.0000 1.0000 proteinGR binding characteristics did not differ between patients and controls or between patients subdivided according to diagnosis or associated clinical features.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7809 10.6902 1.0000 These data suggest that the abnormalities of the HPA system in AD are not related to a proteinGR deficiency .
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3.7930 20.4194 10.7370 Oncogene amplification correlates with dense lymphocyte infiltration in human breast cancers : a role for proteinhematopoietic growth factor release by tumor cells ?
2.2303 20.0783 0.9997 Oncogene amplification correlates with dense lymphocyte infiltration in human breast cancers : a role for hematopoietic growth factor release by cell_typetumor cells ?
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5563 10.4426 0.9999 One hundred six primary breast cancer samples were analysed for c-erbB2 , int-2 , and DNAc-myc gene amplification .
0.8851 1.0000 1.0000 One hundred six primary breast cancer samples were analysed for DNAc-erbB2 , int-2 , and c-myc gene amplification .
0.5763 0.9996 1.0000 One hundred six primary breast cancer samples were analysed for c-erbB2 , DNAint-2 , and c-myc gene amplification .
Cls_Score Left_Reg_Score Right_Reg_Score Text
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3.1344 10.8799 10.6112 Amplified DNAc-erbB2 gene sequences were present in 21.5% of all samples.
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1.8306 10.2990 1.0000 Int-2 was amplified in 13.1% and DNAc-myc was amplified in 10.3%.
0.5352 1.0000 1.0000 proteinInt-2 was amplified in 13.1% and c-myc was amplified in 10.3%.
DNAInt-2 was amplified in 13.1% and c-myc was amplified in 10.3%.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6752 10.1471 1.0000 In a non-parametric test (Kruskal-Wallis) a strong negative association was found between high levels of c-erbB2 amplification and absence of estrogen receptor (ER) (P = .0009) or proteinprogesterone receptor ( PR ) (P = .011) expression.
0.9833 1.0000 1.0000 In a non-parametric test (Kruskal-Wallis) a strong negative association was found between high levels of c-erbB2 amplification and absence of estrogen receptor (ER) (P = .0009) or progesterone receptor ( proteinPR ) (P = .011) expression.
2.3794 20.5310 0.9999 In a non-parametric test (Kruskal-Wallis) a strong negative association was found between high levels of c-erbB2 amplification and absence of proteinestrogen receptor (ER) (P = .0009) or progesterone receptor ( PR ) (P = .011) expression.
1.7287 10.4478 1.0000 In a non-parametric test (Kruskal-Wallis) a strong negative association was found between high levels of proteinc-erbB2 amplification and absence of estrogen receptor (ER) (P = .0009) or progesterone receptor ( PR ) (P = .011) expression.
In a non-parametric test (Kruskal-Wallis) a strong negative association was found between high levels of DNAc-erbB2 amplification and absence of estrogen receptor (ER) (P = .0009) or progesterone receptor ( PR ) (P = .011) expression.
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1.8428 10.2261 1.0000 No correlations were found between all or high levels of amplification of each DNAoncogene separately or combined with T, N, grade, multifocality of tumor , or associated carcinoma in situ.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6475 10.6729 1.0000 There was a trend approaching statistical significance for patients with DNAc-erbB2 amplifications to have positive lymph nodes at surgery (P = 0.09).
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.1283 10.5111 1.0000 A somewhat surprising finding however was a very strong association between DNAoncogene amplification and dense lymphocyte infiltration of the tumor (P = .05). This correlation is even stronger when only high levels of amplification are considered, either for each oncogene separately (P = .0048) or in combination (P = .0007).
1.8707 10.5722 1.0000 A somewhat surprising finding however was a very strong association between oncogene amplification and dense lymphocyte infiltration of the tumor (P = .05). This correlation is even stronger when only high levels of amplification are considered, either for each DNAoncogene separately (P = .0048) or in combination (P = .0007).
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0.9363 1.0000 1.0000 We propose that malignant cell proteincytokine production may help explain this observation.
1.4637 10.3873 0.9999 We propose that proteinmalignant cell cytokine production may help explain this observation.
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3.6791 20.7642 10.7688 Suppression of signals required for activation of proteintranscription factor NF-kappa B in cells constitutively expressing the HTLV-I Tax protein .
3.6356 20.8382 10.6464 Suppression of signals required for activation of transcription factor NF-kappa B in cells constitutively expressing the proteinHTLV-I Tax protein .
0.8458 0.9986 0.9999 Suppression of signals required for activation of transcription factor proteinNF-kappa B in cells constitutively expressing the HTLV-I Tax protein .
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2.0026 20.7076 1.0000 Transient short-term expression of the proteinTax protein of human T-cell leukemia virus type-I ( HTLV-I ) leads to activation of the pleiotropic transcription factor NF-kappa B .
0.9042 0.9955 0.9999 Transient short-term expression of the Tax protein of human T-cell leukemia virus type-I ( HTLV-I ) leads to activation of the pleiotropic transcription factor proteinNF-kappa B .
5.5604 30.4850 10.7076 Transient short-term expression of the Tax protein of human T-cell leukemia virus type-I ( HTLV-I ) leads to activation of the proteinpleiotropic transcription factor NF-kappa B .
Transient short-term expression of the Tax protein of human T-cell leukemia virus type-I ( HTLV-I ) leads to activation of the pleiotropic proteintranscription factor NF-kappa B .
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4.0014 20.9333 10.8787 Consistent with findings obtained with transient expression assays , we observed marked accumulation of the transcription factor NF-kappa B in the nucleus of cell_lineNamalwa B lymphoid cells , which constitutively express Tax .
3.8152 20.9351 10.8046 Consistent with findings obtained with transient expression assays , we observed marked accumulation of the proteintranscription factor NF-kappa B in the nucleus of Namalwa B lymphoid cells , which constitutively express Tax .
0.8888 0.9989 1.0000 Consistent with findings obtained with transient expression assays , we observed marked accumulation of the transcription factor proteinNF-kappa B in the nucleus of Namalwa B lymphoid cells , which constitutively express Tax .
0.7769 1.0000 1.0000 Consistent with findings obtained with transient expression assays , we observed marked accumulation of the transcription factor NF-kappa B in the nucleus of Namalwa B lymphoid cells , which constitutively express proteinTax .
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3.7628 20.4261 10.1911 In contrast, NF-kappa B activity was not detected in the nucleus following long-term expression of Tax in cell_lineJurkat T lymphocytes .
2.3007 20.2261 1.0000 In contrast, proteinNF-kappa B activity was not detected in the nucleus following long-term expression of Tax in Jurkat T lymphocytes .
1.5947 10.7797 1.0000 In contrast, NF-kappa B activity was not detected in the nucleus following long-term expression of proteinTax in Jurkat T lymphocytes .
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2.2631 20.1481 0.9999 The ability of both mitogens and cytokines to activate NF-kappa B was also blocked in cell_lineJurkat cells constitutively expressing Tax .
1.5614 10.8269 1.0000 The ability of both mitogens and cytokines to activate NF-kappa B was also blocked in Jurkat cells constitutively expressing proteinTax .
1.4991 10.7916 1.0000 The ability of both mitogens and cytokines to activate proteinNF-kappa B was also blocked in Jurkat cells constitutively expressing Tax .
0.9367 1.0000 1.0000 The ability of both mitogens and proteincytokines to activate NF-kappa B was also blocked in Jurkat cells constitutively expressing Tax .
0.7727 0.9996 1.0000 The ability of both proteinmitogens and cytokines to activate NF-kappa B was also blocked in Jurkat cells constitutively expressing Tax .
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2.8882 20.3935 10.5804 However, the activation of other proteinmitogen-inducible transcription factors , such as Fos and Jun , was unaffected.
1.5750 10.2202 1.0000 However, the activation of other mitogen-inducible transcription factors , such as proteinFos and Jun , was unaffected.
0.8978 1.0000 1.0000 However, the activation of other mitogen-inducible transcription factors , such as Fos and proteinJun , was unaffected.
0.6985 0.9998 0.9999 However, the activation of other mitogen-inducible proteintranscription factors , such as Fos and Jun , was unaffected.
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1.7956 10.5419 1.0000 Thus, depending on the cellular environment , the short- and long-term effects of proteinTax expression can be quite different.
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1.7859 10.3710 1.0000 Consequently, one function of proteinTax in cells infected with HTLV-I might involve cell-type-specific suppression , as opposed to activation, of distinct signal pathways .
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1.6746 10.0002 0.9998 The cell_linecells lines described here should be useful for the delineation of signaling pathways utilized in the selective regulation of gene expression .
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0.9690 1.0000 1.0000 proteinInterferon-gamma and the sexual dimorphism of autoimmunity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9669 20.0577 1.0000 The sexual difference in the incidence of proteinautoimmune diseases has remained an enigma for many years.
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0.9282 1.0000 1.0000 In the examination of the induction of autoimmunity in transgenic mice , evidence has been obtained further implicating the lymphokine proteininterferon-gamma in the etiology of autoimmunity .
2.4544 20.9011 1.0000 In the examination of the induction of autoimmunity in transgenic mice , evidence has been obtained further implicating the proteinlymphokine interferon-gamma in the etiology of autoimmunity .
In the examination of the induction of autoimmunity in transgenic mice , evidence has been obtained further implicating the proteinlymphokine interferon-gamma in the etiology of autoimmunity .
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1.7663 10.5278 1.0000 Sex steroid regulation of the production of this molecule, as well as other proteincytokines , may help explain the gender-specific differences in the immune system , including autoimmunity .
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2.9191 10.9449 10.4913 Cloning of a transcriptionally active proteinhuman TATA binding factor .
Cloning of a proteintranscriptionally active human TATA binding factor .
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3.9552 30.1712 10.7944 Transcription factor IID ( TFIID ) binds to the TATA box promoter element and regulates the expression of most eukaryotic genes transcribed by proteinRNA polymerase II .
3.7422 20.9405 10.6650 Transcription factor IID ( TFIID ) binds to the DNATATA box promoter element and regulates the expression of most eukaryotic genes transcribed by RNA polymerase II .
1.5846 0.9981 10.3815 proteinTranscription factor IID ( TFIID ) binds to the TATA box promoter element and regulates the expression of most eukaryotic genes transcribed by RNA polymerase II .
1.1591 10.8633 0.9999 Transcription factor IID ( TFIID ) binds to the TATA box promoter element and regulates the expression of most DNAeukaryotic genes transcribed by RNA polymerase II .
0.9714 1.0000 1.0000 Transcription factor IID ( proteinTFIID ) binds to the TATA box promoter element and regulates the expression of most eukaryotic genes transcribed by RNA polymerase II .
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2.9765 20.3870 10.0872 Complementary DNA ( cDNA ) encoding a proteinhuman TFIID protein has been cloned.
0.9309 1.0000 1.0000 Complementary DNA ( DNAcDNA ) encoding a human TFIID protein has been cloned.
0.9165 1.0000 0.9841 Complementary DNA ( cDNA ) encoding a human proteinTFIID protein has been cloned.
0.7816 0.9988 0.9998 DNAComplementary DNA ( cDNA ) encoding a human TFIID protein has been cloned.
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3.1658 10.7866 10.2450 The proteinhuman TFIID polypeptide has 339 amino acids and a molecular size of 37,745 daltons .
0.9429 1.0000 0.9830 The human proteinTFIID polypeptide has 339 amino acids and a molecular size of 37,745 daltons .
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2.9277 30.2597 0.9999 The carboxyl-terminal 181 amino acids of the proteinhuman TFIID protein shares 80% identity with the TFIID protein from Saccharomyces cerevisiae .
1.7783 20.6995 0.9865 The carboxyl-terminal 181 amino acids of the human TFIID protein shares 80% identity with the proteinTFIID protein from Saccharomyces cerevisiae .
1.5470 10.4491 0.9982 The proteincarboxyl-terminal 181 amino acids of the human TFIID protein shares 80% identity with the TFIID protein from Saccharomyces cerevisiae .
0.9068 1.0000 0.9858 The carboxyl-terminal 181 amino acids of the human proteinTFIID protein shares 80% identity with the TFIID protein from Saccharomyces cerevisiae .
1.8697 20.8956 1.0000 The carboxyl-terminal 181 amino acids of the human TFIID protein shares 80% identity with the proteinTFIID protein from Saccharomyces cerevisiae .
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2.2004 20.4643 0.9999 The amino terminus contains an unusual repeat of 38 consecutive glutamine residues and an proteinX-Thr-Pro repeat .
0.7347 0.9951 1.0000 The proteinamino terminus contains an unusual repeat of 38 consecutive glutamine residues and an X-Thr-Pro repeat .
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Expression of DNADNA in reticulocyte lysates or in Escherichia coli yielded a protein that was competent for both DNA binding and transcription activation .
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3.4263 20.2766 10.6660 A novel T-cell trans-activator that recognizes a DNAphorbol ester-inducible element of the interleukin-2 promoter .
2.5645 20.1427 10.1068 A novel proteinT-cell trans-activator that recognizes a phorbol ester-inducible element of the interleukin-2 promoter .
1.9565 20.1914 0.9997 A novel T-cell trans-activator that recognizes a phorbol ester-inducible element of the DNAinterleukin-2 promoter .
A novel T-cell trans-activator that recognizes a phorbol ester-inducible element of the proteininterleukin-2 promoter .
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1.7176 10.4143 0.9702 The DNAinterleukin 2 ( IL-2 ) gene promoter is recognized by several cell-type-specific and ubiquitous transcriptional regulators that integrate information transmitted by various signaling systems leading to IL-2 production and T-cell activation .
1.6149 10.0296 1.0000 The interleukin 2 ( IL-2 ) gene promoter is recognized by several cell-type-specific and ubiquitous transcriptional regulators that integrate information transmitted by various signaling systems leading to proteinIL-2 production and T-cell activation .
0.9721 1.0000 0.9967 The interleukin 2 ( proteinIL-2 ) gene promoter is recognized by several cell-type-specific and ubiquitous transcriptional regulators that integrate information transmitted by various signaling systems leading to IL-2 production and T-cell activation .
The proteininterleukin 2 ( IL-2 ) gene promoter is recognized by several cell-type-specific and ubiquitous transcriptional regulators that integrate information transmitted by various signaling systems leading to IL-2 production and T-cell activation .
The interleukin 2 ( IL-2 ) gene promoter is recognized by several cell-type-specific and ubiquitous transcriptional regulators that integrate information transmitted by various signaling systems leading to IL-2 production and cell_typeT-cell activation .
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3.6767 20.7855 10.6643 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator TCF-1 (for T-Cell Factor-1 ), which recognizes a DNAT-cell-specific response element ( TCE ) located within the IL-2 promoter .
2.1407 20.5072 0.9999 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator TCF-1 (for T-Cell Factor-1 ), which recognizes a T-cell-specific response element ( TCE ) located within the DNAIL-2 promoter .
1.7199 20.4812 0.9842 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator TCF-1 (for T-Cell Factor-1 ), which recognizes a T-cell-specific response element ( TCE ) located within the proteinIL-2 promoter .
0.9628 0.9999 1.0000 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator proteinTCF-1 (for T-Cell Factor-1 ), which recognizes a T-cell-specific response element ( TCE ) located within the IL-2 promoter .
0.9505 1.0000 1.0000 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator TCF-1 (for T-Cell Factor-1 ), which recognizes a T-cell-specific response element ( DNATCE ) located within the IL-2 promoter .
0.8314 0.9998 1.0000 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel T-cell-specific transcriptional activator TCF-1 (for proteinT-Cell Factor-1 ), which recognizes a T-cell-specific response element ( TCE ) located within the IL-2 promoter .
3.6999 20.6830 10.9336 Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the novel proteinT-cell-specific transcriptional activator TCF-1 (for T-Cell Factor-1 ), which recognizes a T-cell-specific response element ( TCE ) located within the IL-2 promoter .
Using a combination of transfection , protein-DNA binding, and in vitro transcription methods , we have discovered the proteinnovel T-cell-specific transcriptional activator TCF-1 (for T-Cell Factor-1 ), which recognizes a T-cell-specific response element ( TCE ) located within the IL-2 promoter .
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5.0813 20.9216 20.6374 Although the TCE is similar in sequence to a DNAconsensus NF kappa B site , several criteria indicate that TCF-1 is distinct from NF kappa B .
3.2720 20.9028 10.7388 Although the TCE is similar in sequence to a consensus NF kappa B site , several criteria indicate that TCF-1 is distinct from proteinNF kappa B .
1.6638 10.9682 1.0000 Although the DNATCE is similar in sequence to a consensus NF kappa B site , several criteria indicate that TCF-1 is distinct from NF kappa B .
1.4016 1.0000 10.5572 Although the TCE is similar in sequence to a consensus proteinNF kappa B site , several criteria indicate that TCF-1 is distinct from NF kappa B .
0.8193 1.0000 1.0000 Although the TCE is similar in sequence to a consensus NF kappa B site , several criteria indicate that proteinTCF-1 is distinct from NF kappa B .
0.5579 0.9973 0.9979 Although the TCE is similar in sequence to a consensus DNANF kappa B site , several criteria indicate that TCF-1 is distinct from NF kappa B .
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3.4322 20.4939 10.8061 However, like proteinNF kappa B , TCF-1 activity is induced by phorbol esters and other T-cell activators .
0.9140 1.0000 1.0000 However, like NF kappa B , proteinTCF-1 activity is induced by phorbol esters and other T-cell activators .
1.9231 20.2033 0.9998 However, like NF kappa B , TCF-1 activity is induced by phorbol esters and other proteinT-cell activators .
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1.7908 10.8815 1.0000 Monofactorial analysis identified the following factors to be correlated with increased risk: moderate/marked mononuclear cell reaction ( MCR ), high histologic grade (G), extensive intraductal component ( EIC ), tumor necrosis , macroscopic multiplicity , proteinestrogen receptor negativity , anatomic tumor size , age younger than 40 years, and vascular invasion .
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3.9737 20.6798 10.4326 Tax -independent binding of multiple cellular factors to DNATax -response element DNA of HTLV-I .
1.3554 10.3809 0.9945 Tax -independent binding of multiple cellular factors to proteinTax -response element DNA of HTLV-I .
1.2939 10.8386 0.9996 Tax -independent binding of multiple proteincellular factors to Tax -response element DNA of HTLV-I .
0.9685 1.0000 1.0000 proteinTax -independent binding of multiple cellular factors to Tax -response element DNA of HTLV-I .
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3.5665 30.1612 10.8286 The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as TRE ( DNATax -response element ) that is responsive to the virally encoded transactivator protein Tax .
2.4712 10.1042 10.1236 The DNAhuman T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as TRE ( Tax -response element ) that is responsive to the virally encoded transactivator protein Tax .
2.1076 40.9029 10.0160 The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as TRE ( Tax -response element ) that is responsive to the proteinvirally encoded transactivator protein Tax .
1.6057 10.0379 0.9987 The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as TRE ( proteinTax -response element ) that is responsive to the virally encoded transactivator protein Tax .
1.5669 10.6537 1.0000 The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as DNATRE ( Tax -response element ) that is responsive to the virally encoded transactivator protein Tax .
0.9593 0.9998 1.0000 The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a 21-base pair sequence designated here as TRE ( Tax -response element ) that is responsive to the virally encoded transactivator protein proteinTax .
2.1281 20.6393 10.9558 The human T-cell leukemia virus type I ( HTLV-I ) promoter contains three copies of imperfect repeats of a DNA21-base pair sequence designated here as TRE ( Tax -response element ) that is responsive to the virally encoded transactivator protein Tax .
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6.0864 20.8312 20.1648 We have identified and separated four nuclear proteins from C81-66-45 cells, an cell_lineHTLV-I immortalized Tax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the TRE -DNA , none of which are identical with the Tax -protein .
2.1046 20.5265 0.9927 We have identified and separated four nuclear proteins from C81-66-45 cells, an HTLV-I immortalized Tax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the TRE -DNA , none of which are identical with the proteinTax -protein .
1.9981 20.2603 0.9941 We have identified and separated four nuclear proteins from C81-66-45 cells, an HTLV-I immortalized Tax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the DNATRE -DNA , none of which are identical with the Tax -protein .
1.8874 20.0843 1.0000 We have identified and separated four nuclear proteins from C81-66-45 cells, an HTLV-I immortalized Tax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the DNATRE -DNA , none of which are identical with the Tax -protein .
1.8292 20.7799 0.9999 We have identified and separated four nuclear proteins from C81-66-45 cells, an HTLV-I immortalized Tax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the TRE -DNA , none of which are identical with the proteinTax -protein .
1.3887 10.6008 0.9999 We have identified and separated four proteinnuclear proteins from C81-66-45 cells, an HTLV-I immortalized Tax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the TRE -DNA , none of which are identical with the Tax -protein .
0.9588 1.0000 0.9985 We have identified and separated four nuclear proteins from C81-66-45 cells, an HTLV-I immortalized proteinTax -expressing human T-lymphocyte line (Salahuddin et al., 1983), that interact with the TRE -DNA , none of which are identical with the Tax -protein .
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3.9046 20.0891 10.9516 First, from different cell lines three or all four of the nuclear proteins were specifically cross-linked by UV irradiation to the radioactively labeled DNATRE -DNA fragment .
1.5385 10.9798 1.0000 First, from different cell lines three or all four of the proteinnuclear proteins were specifically cross-linked by UV irradiation to the radioactively labeled TRE -DNA fragment .
0.8561 1.0000 0.9955 First, from different cell lines three or all four of the nuclear proteins were specifically cross-linked by UV irradiation to the radioactively labeled DNATRE -DNA fragment .
2.3434 20.1965 0.9999 First, from different cell_linecell lines three or all four of the nuclear proteins were specifically cross-linked by UV irradiation to the radioactively labeled TRE -DNA fragment .
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3.3385 10.9552 10.5608 Second, proteinTRE -DNA binding proteins sedimented through a glycerol density gradient at rates corresponding to proteins of native molecular weights of 35 to 50 kD and 110 kD.
0.8207 1.0000 0.9946 Second, DNATRE -DNA binding proteins sedimented through a glycerol density gradient at rates corresponding to proteins of native molecular weights of 35 to 50 kD and 110 kD.
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2.8359 20.9026 10.9201 Third, only the protein50 kD protein was retained on a biotinylated DNA-streptavidin matrix when the DNA fragment contained the TRE -DNA .
2.1787 20.7580 0.9875 Third, only the 50 kD protein was retained on a biotinylated DNA-streptavidin matrix when the DNA fragment contained the DNATRE -DNA .
2.0679 20.4933 0.9998 Third, only the 50 kD protein was retained on a biotinylated DNA-streptavidin matrix when the DNA fragment contained the DNATRE -DNA .
1.8449 20.2297 0.9998 Third, only the 50 kD protein was retained on a biotinylated DNA-streptavidin matrix when the DNADNA fragment contained the TRE -DNA .
1.5056 20.1384 0.9999 Third, only the 50 kD protein was retained on a proteinbiotinylated DNA-streptavidin matrix when the DNA fragment contained the TRE -DNA .
0.7239 1.0000 1.0000 Third, only the 50 kD protein was retained on a biotinylated proteinDNA-streptavidin matrix when the DNA fragment contained the TRE -DNA .
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4.6973 30.1807 10.5114 Fourth, extensive purification by several cycles of TRE -DNA affinity chromatography resulted in the 32 , 36 to 42 and 110 kD proteins and to less extent the protein50 kD factor .
1.8039 10.5070 1.0000 Fourth, extensive purification by several cycles of DNATRE -DNA affinity chromatography resulted in the 32 , 36 to 42 and 110 kD proteins and to less extent the 50 kD factor .
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1.3910 10.3630 1.0000 Two abundant proteins of 75 and 80 kD were competed out by DNApoly[d(I-C)] in all reactions.
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3.5541 30.2652 10.0017 The cAMP-response element CRE , TGACGTCA , present in the DNA21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two G 's destroys this complex.
0.9473 0.9998 0.9996 The cAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- DNATRE -DNA interactions because mutation of the two G 's destroys this complex.
0.6788 0.9995 1.0000 The cAMP-response element DNACRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two G 's destroys this complex.
2.4299 10.4251 10.1820 The DNAcAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two G 's destroys this complex.
0.7507 0.9995 1.0000 The cAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two DNAG 's destroys this complex.
0.6103 0.9999 0.9676 The cAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two DNAG 's destroys this complex.
0.5595 0.9982 0.9999 The cAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- DNATRE -DNA interactions because mutation of the two G 's destroys this complex.
The DNAcAMP-response element CRE , TGACGTCA , present in the 21 base-pair sequence , appears to be essential for specific protein- TRE -DNA interactions because mutation of the two G 's destroys this complex.
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5.2567 30.6748 10.9626 This result suggests that the proteincAMP response element binding protein , CREB , is involved in the protein- TRE -DNA complex and in mediating the Tax response .
4.1960 30.3306 10.8652 This result suggests that the cAMP response element binding protein , CREB , is involved in the proteinprotein- TRE -DNA complex and in mediating the Tax response .
1.5531 10.2064 1.0000 This result suggests that the cAMP response element binding protein , CREB , is involved in the protein- TRE -DNA complex and in mediating the proteinTax response .
0.9226 1.0000 1.0000 This result suggests that the cAMP response element binding protein , proteinCREB , is involved in the protein- TRE -DNA complex and in mediating the Tax response .
0.8452 1.0000 0.9858 This result suggests that the cAMP response element binding protein , CREB , is involved in the protein- DNATRE -DNA complex and in mediating the Tax response .
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1.6849 20.3441 0.9999 Two distinct proteintranscription factors that bind the immunoglobulin enhancer microE5/kappa 2 motif .
1.5338 20.6831 0.9821 Two distinct transcription factors that bind the DNAimmunoglobulin enhancer microE5/kappa 2 motif .
4.4562 20.9947 10.8451 Two distinct transcription factors that bind the DNAimmunoglobulin enhancer microE5/kappa 2 motif .
Two distinct transcription factors that bind the immunoglobulin enhancer DNAmicroE5/kappa 2 motif .
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5.7718 20.9783 20.8099 Activity of the DNAimmunoglobulin heavy and kappa light chain gene enhancers depends on a complex interplay of ubiquitous and developmentally regulated proteins .
Activity of the immunoglobulin heavy and kappa light chain gene enhancers depends on a complex interplay of proteinubiquitous and developmentally regulated proteins .
Activity of the immunoglobulin heavy and kappa light chain gene enhancers depends on a complex interplay of ubiquitous and proteindevelopmentally regulated proteins .
Activity of the immunoglobulin heavy and kappa light chain gene enhancers depends on a complex interplay of proteinubiquitous and developmentally regulated proteins .
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3.8702 20.8606 10.6135 Two complementary DNAs were isolated that encode proteins, denoted ITF-1 and ITF-2 , that are expressed in a variety of cell types and bind the DNAmicroE5/kappa 2 motif found in both heavy and kappa light chain enhancers .
1.6169 10.9062 1.0000 Two DNAcomplementary DNAs were isolated that encode proteins, denoted ITF-1 and ITF-2 , that are expressed in a variety of cell types and bind the microE5/kappa 2 motif found in both heavy and kappa light chain enhancers .
0.9696 1.0000 1.0000 Two complementary DNAs were isolated that encode proteins, denoted ITF-1 and proteinITF-2 , that are expressed in a variety of cell types and bind the microE5/kappa 2 motif found in both heavy and kappa light chain enhancers .
0.8913 1.0000 1.0000 Two complementary DNAs were isolated that encode proteins, denoted proteinITF-1 and ITF-2 , that are expressed in a variety of cell types and bind the microE5/kappa 2 motif found in both heavy and kappa light chain enhancers .
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1.6968 10.5196 1.0000 The DNAcomplementary DNAs are the products of distinct genes, yet both ITF-1 and ITF-2 are structurally and functionally similar.
1.6796 10.3886 1.0000 The complementary DNAs are the products of distinct genes, yet both proteinITF-1 and ITF-2 are structurally and functionally similar.
0.9281 1.0000 1.0000 The complementary DNAs are the products of distinct genes, yet both ITF-1 and proteinITF-2 are structurally and functionally similar.
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2.4511 20.0589 1.0000 The two proteins interact with one another through their putative proteinhelix-loop-helix motifs and each possesses a distinct domain that dictates transcription activation .
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3.7047 20.4423 10.6416 Elevated glucocorticoid receptor concentrations before and after glucocorticoid therapy in cell_typeperipheral mononuclear leukocytes of patients with atopic dermatitis .
1.5099 10.5981 1.0000 Elevated proteinglucocorticoid receptor concentrations before and after glucocorticoid therapy in peripheral mononuclear leukocytes of patients with atopic dermatitis .
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4.0403 20.2013 10.3074 The number and affinity of glucocorticoid binding sites in cell_typeperipheral mononuclear leukocytes of patients with atopic dermatitis ( AD ) and healthy controls were determined under baseline conditions and after a defined oral glucocorticoid treatment .
3.8912 20.7805 10.7463 The number and affinity of proteinglucocorticoid binding sites in peripheral mononuclear leukocytes of patients with atopic dermatitis ( AD ) and healthy controls were determined under baseline conditions and after a defined oral glucocorticoid treatment .
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1.6402 10.9459 1.0000 Patients with AD (n = 15) exhibited significantly more proteinglucocorticoid receptors ( GR ) per cell than the control group (n = 22), while the GR affinity did not differ.
0.9757 1.0000 1.0000 Patients with AD (n = 15) exhibited significantly more glucocorticoid receptors ( proteinGR ) per cell than the control group (n = 22), while the GR affinity did not differ.
0.9503 1.0000 1.0000 Patients with AD (n = 15) exhibited significantly more glucocorticoid receptors ( GR ) per cell than the control group (n = 22), while the proteinGR affinity did not differ.
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2.4456 20.6212 0.9948 Methylprednisolone treatment resulted in a significant reduction of the proteinGR sites per cell in the steroid-treated control group (n = 10) in contrast to the patients .
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0.9762 1.0000 1.0000 In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity , the elevated GR concentrations in AD lend support to the hypothesis of a compensatory GR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP -induced proteinGR expression .
0.9586 1.0000 1.0000 In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity , the elevated GR concentrations in AD lend support to the hypothesis of a compensatory proteinGR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP -induced GR expression .
0.9577 1.0000 1.0000 In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity , the elevated proteinGR concentrations in AD lend support to the hypothesis of a compensatory GR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP -induced GR expression .
0.9035 1.0000 1.0000 In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and proteincAMP-phosphodiesterase activity , the elevated GR concentrations in AD lend support to the hypothesis of a compensatory GR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP -induced GR expression .
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1.5125 20.5353 0.9999 The actions of cyclosporin A and FK506 suggest a novel step in the activation of cell_typeT lymphocytes .
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1.7097 10.5844 1.0000 Cyclosporin A and FK506 are immunosuppressive compounds that have similar inhibitory effects on the expression of several proteinlymphokines produced by T lymphocytes .
1.5757 10.5693 0.9998 Cyclosporin A and FK506 are immunosuppressive compounds that have similar inhibitory effects on the expression of several lymphokines produced by cell_typeT lymphocytes .
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2.3518 20.4657 1.0000 Despite their similar effects the drugs bind to two different proteincytosolic protein , cyclophilin and FKBP respectively, which raises the possibility that they have different modes of action.
0.9605 1.0000 1.0000 Despite their similar effects the drugs bind to two different cytosolic protein , cyclophilin and proteinFKBP respectively, which raises the possibility that they have different modes of action.
0.9591 1.0000 1.0000 Despite their similar effects the drugs bind to two different cytosolic protein , proteincyclophilin and FKBP respectively, which raises the possibility that they have different modes of action.
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3.8328 20.9254 10.5462 Using constructs in which mRNA production controlled by a specific transcription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by NF-AT , NFIL2 A , NFIL2 B and partially inhibited transcription activated by proteinNF kappa B .
2.3239 20.0452 1.0000 Using constructs in which mRNA production controlled by a specific proteintranscription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by NF-AT , NFIL2 A , NFIL2 B and partially inhibited transcription activated by NF kappa B .
1.6724 10.6730 1.0000 Using constructs in which mRNA production controlled by a specific transcription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by NF-AT , NFIL2 A , proteinNFIL2 B and partially inhibited transcription activated by NF kappa B .
1.6705 10.6657 1.0000 Using constructs in which mRNA production controlled by a specific transcription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by NF-AT , proteinNFIL2 A , NFIL2 B and partially inhibited transcription activated by NF kappa B .
1.5506 10.1423 1.0000 Using constructs in which RNAmRNA production controlled by a specific transcription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by NF-AT , NFIL2 A , NFIL2 B and partially inhibited transcription activated by NF kappa B .
0.8878 0.9998 1.0000 Using constructs in which mRNA production controlled by a specific transcription factor could be readily measured we found that both cyclosporin A and FK506 completely inhibited transcription activated by proteinNF-AT , NFIL2 A , NFIL2 B and partially inhibited transcription activated by NF kappa B .
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2.5800 20.2922 1.0000 However, cyclosporin A and FK506 did not inhibit Ca2+ mobilization dependent expression of RNAc-fos mRNA indicating that only a subset of signalling pathways regulated by Ca2+ is sensitive to these drugs.
1.8444 20.5317 0.9905 However, cyclosporin A and FK506 did not inhibit Ca2+ mobilization dependent expression of DNAc-fos mRNA indicating that only a subset of signalling pathways regulated by Ca2+ is sensitive to these drugs.
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2.5760 20.5608 1.0000 Furthermore, we did not observe any qualitative differences between the effect of cyclosporin A and FK506 on six different transcription factors which suggests that these drugs may interfere with the activity of a novel Ca2+ dependent step that regulates several proteintranscription factors .
2.5725 20.2346 1.0000 Furthermore, we did not observe any qualitative differences between the effect of cyclosporin A and FK506 on six different proteintranscription factors which suggests that these drugs may interfere with the activity of a novel Ca2+ dependent step that regulates several transcription factors .
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5.0057 20.4862 20.7367 The internal methionine codons of DNAhuman T-cell leukemia virus type II rex gene are not required for p24rex production or virus replication and transformation .
0.7808 1.0000 1.0000 The internal methionine codons of human T-cell leukemia virus type II rex gene are not required for proteinp24rex production or virus replication and transformation .
1.0890 10.2612 0.9886 The DNAinternal methionine codons of human T-cell leukemia virus type II rex gene are not required for p24rex production or virus replication and transformation .
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4.7823 20.8695 10.5586 Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two DNAnonstructural trans-acting regulatory genes , tax and rex , located in the 3' region of the viral genome .
2.1962 20.2474 0.9998 Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two nonstructural trans-acting regulatory genes , tax and rex , located in the 3' region of the DNAviral genome .
2.1737 20.4543 0.9999 Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two nonstructural trans-acting regulatory genes , tax and rex , located in the DNA3' region of the viral genome .
0.9465 1.0000 1.0000 Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two nonstructural trans-acting regulatory genes , tax and DNArex , located in the 3' region of the viral genome .
0.9336 1.0000 1.0000 Human T-cell leukemia virus types I ( HTLV-I ) and II ( HTLV-II ) have two nonstructural trans-acting regulatory genes , DNAtax and rex , located in the 3' region of the viral genome .
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3.8012 20.5404 10.5279 The tax gene product ( HTLV-I p40tax and HTLV-II p37tax ) is the transcriptional activator of the DNAviral long terminal repeat .
2.6887 10.6867 10.7949 The proteintax gene product ( HTLV-I p40tax and HTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .
1.5257 10.4371 1.0000 The tax gene product ( proteinHTLV-I p40tax and HTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .
1.2025 10.0601 1.0000 The tax gene product ( HTLV-I p40tax and proteinHTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .
1.9455 20.1179 1.0000 The tax gene product ( HTLV-I p40tax and HTLV-II p37tax ) is the proteintranscriptional activator of the viral long terminal repeat .
0.8349 1.0000 1.0000 The tax gene product ( HTLV-I p40tax and HTLV-II proteinp37tax ) is the transcriptional activator of the viral long terminal repeat .
0.6935 1.0000 1.0000 The tax gene product ( HTLV-I proteinp40tax and HTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .
The tax gene product ( HTLV-I DNAp40tax and HTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .
The tax gene product ( HTLV-I p40tax and HTLV-II DNAp37tax ) is the transcriptional activator of the viral long terminal repeat .
The DNAtax gene product ( HTLV-I p40tax and HTLV-II p37tax ) is the transcriptional activator of the viral long terminal repeat .
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1.7687 10.3740 1.0000 The rex gene encodes two protein products, p27rex /p21rex and proteinp26rex /p24rex in HTLV-I and HTLV-II , respectively.
1.5966 10.3129 1.0000 The DNArex gene encodes two protein products, p27rex /p21rex and p26rex /p24rex in HTLV-I and HTLV-II , respectively.
1.1732 10.5009 0.9909 The rex gene encodes two protein products, p27rex /p21rex and proteinp26rex /p24rex in HTLV-I and HTLV-II , respectively.
0.9135 0.9995 1.0000 The rex gene encodes two protein products, proteinp27rex /p21rex and p26rex /p24rex in HTLV-I and HTLV-II , respectively.
0.7495 1.0000 1.0000 The rex gene encodes two protein products, p27rex /p21rex and p26rex protein/p24rex in HTLV-I and HTLV-II , respectively.
0.6938 0.9998 0.9893 The rex gene encodes two protein products, proteinp27rex /p21rex and p26rex /p24rex in HTLV-I and HTLV-II , respectively.
0.6515 1.0000 1.0000 The rex gene encodes two protein products, p27rex protein/p21rex and p26rex /p24rex in HTLV-I and HTLV-II , respectively.
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1.5675 10.9506 0.9999 Rex acts posttranscriptionally to facilitate accumulation of full-length gag/pol and singly spliced RNAenv mRNA in the cytoplasm of HTLV-infected cells .
1.5166 10.8354 0.9997 Rex acts posttranscriptionally to facilitate accumulation of full-length gag/pol and singly spliced env mRNA in the cytoplasm of cell_typeHTLV-infected cells .
0.9706 1.0000 1.0000 proteinRex acts posttranscriptionally to facilitate accumulation of full-length gag/pol and singly spliced env mRNA in the cytoplasm of HTLV-infected cells .
Rex acts posttranscriptionally to facilitate accumulation of full-length proteingag/pol and singly spliced env mRNA in the cytoplasm of HTLV-infected cells .
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2.2685 20.1070 1.0000 Previous studies showed that the first ATG of the DNArex gene is critical for Rex production and function.
1.7678 10.1719 1.0000 Previous studies showed that the first ATG of the rex gene is critical for proteinRex production and function.
Previous studies showed that the first ATG of the DNArex gene is critical for Rex production and function.
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0.8833 1.0000 1.0000 The importance of the internal ATGs to proteinRex function is not known.
0.9246 1.0000 1.0000 The importance of the internal DNAATGs to Rex function is not known.
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3.5161 20.7281 10.7299 However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the RNAtax /rex mRNA .
1.7275 10.1019 1.0000 However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that proteinp21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the tax /rex mRNA .
0.9333 1.0000 1.0000 However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II proteinp24rex , results from initiation at an internal AUG of the tax /rex mRNA .
3.9097 20.5705 10.9377 However, in vitro mutagenesis of the DNAHTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the tax /rex mRNA .
1.4380 10.6762 1.0000 However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy proteinHTLV-II p24rex , results from initiation at an internal AUG of the tax /rex mRNA .
However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the DNAtax /rex mRNA .
However, in vitro mutagenesis of the HTLV-I DNArex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the tax /rex mRNA .
However, in vitro mutagenesis of the HTLV-I rex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the tax DNA/rex mRNA .
However, in vitro mutagenesis of the HTLV-I DNArex gene has provided indirect evidence which suggests that p21rex , and by analogy HTLV-II p24rex , results from initiation at an internal AUG of the tax /rex mRNA .
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1.5814 10.6901 0.9999 By using an infectious molecular clone of HTLV-II , we investigated the importance of the internal ATGs of the DNArex gene on Rex protein production and function.
1.3080 10.9795 0.9907 By using an infectious molecular clone of HTLV-II , we investigated the importance of the internal ATGs of the rex gene on proteinRex protein production and function.
1.6781 10.5505 1.0000 By using an infectious molecular clone of HTLV-II , we investigated the importance of the internal ATGs of the rex gene on proteinRex protein production and function.
1.1736 10.9797 0.9999 By using an infectious molecular clone of HTLV-II , we investigated the importance of the DNAinternal ATGs of the rex gene on Rex protein production and function.
By using an infectious molecular clone of HTLV-II , we investigated the importance of the internal ATGs of the DNArex gene on Rex protein production and function.
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2.2953 20.9059 0.9999 Our results indicate that p24rex of HTLV-II is not initiated at an internal AUG and that the internal methionine codons are not crucial to the function of the DNArex gene and, ultimately, the transforming properties of the virus .
1.7122 10.5252 1.0000 Our results indicate that proteinp24rex of HTLV-II is not initiated at an internal AUG and that the internal methionine codons are not crucial to the function of the rex gene and, ultimately, the transforming properties of the virus .
3.8241 20.8125 10.6536 Our results indicate that p24rex of HTLV-II is not initiated at an internal AUG and that the DNAinternal methionine codons are not crucial to the function of the rex gene and, ultimately, the transforming properties of the virus .
1.8748 20.2928 1.0000 Our results indicate that p24rex of HTLV-II is not initiated at an DNAinternal AUG and that the internal methionine codons are not crucial to the function of the rex gene and, ultimately, the transforming properties of the virus .
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4.7625 20.6839 10.9144 Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous Oct-1 and proteinB cell type Oct-2 proteins .
4.1235 20.5560 10.8125 Astrocytes and glioblastoma cells express novel proteinoctamer-DNA binding proteins distinct from the ubiquitous Oct-1 and B cell type Oct-2 proteins .
2.5963 10.7137 10.9792 Astrocytes and cell_typeglioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous Oct-1 and B cell type Oct-2 proteins .
1.2887 10.8532 0.9997 Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the proteinubiquitous Oct-1 and B cell type Oct-2 proteins .
0.9125 1.0000 0.9998 cell_typeAstrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous Oct-1 and B cell type Oct-2 proteins .
0.7662 1.0000 0.9999 Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous proteinOct-1 and B cell type Oct-2 proteins .
0.7353 1.0000 0.9103 Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous Oct-1 and B cell type proteinOct-2 proteins .
0.6495 0.9927 0.9996 Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the ubiquitous Oct-1 and B cell type proteinOct-2 proteins .
Astrocytes and glioblastoma cells express novel octamer-DNA binding proteins distinct from the proteinubiquitous Oct-1 and B cell type Oct-2 proteins .
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2.2788 20.6239 1.0000 The 'octamer' sequence , ATGCAAAT or its complement ATTTGCAT , is a key element for the transcriptional regulation of DNAimmunoglobulin genes in B-lymphocytes as well as a number of housekeeping genes in all cell types.
2.2358 20.2942 1.0000 The 'octamer' sequence , ATGCAAAT or its complement ATTTGCAT , is a key element for the transcriptional regulation of immunoglobulin genes in B-lymphocytes as well as a number of DNAhousekeeping genes in all cell types.
1.5635 10.8696 1.0000 The DNA'octamer' sequence , ATGCAAAT or its complement ATTTGCAT , is a key element for the transcriptional regulation of immunoglobulin genes in B-lymphocytes as well as a number of housekeeping genes in all cell types.
0.8858 1.0000 1.0000 The 'octamer' sequence , ATGCAAAT or its complement ATTTGCAT , is a key element for the transcriptional regulation of immunoglobulin genes in cell_typeB-lymphocytes as well as a number of housekeeping genes in all cell types.
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2.2530 20.4144 1.0000 In lymphocytes , the octamer-binding protein Oct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the ubiquitous protein Oct-1 seems to control general DNAoctamer site -dependent transcription .
2.1285 20.9703 0.9956 In lymphocytes , the proteinoctamer-binding protein Oct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the ubiquitous protein Oct-1 seems to control general octamer site -dependent transcription .
1.8137 10.0889 1.0000 In cell_typelymphocytes , the octamer-binding protein Oct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the ubiquitous protein Oct-1 seems to control general octamer site -dependent transcription .
0.9893 1.0000 1.0000 In lymphocytes , the octamer-binding protein proteinOct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the ubiquitous protein Oct-1 seems to control general octamer site -dependent transcription .
2.0264 20.9490 0.9950 In lymphocytes , the octamer-binding protein Oct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the proteinubiquitous protein Oct-1 seems to control general octamer site -dependent transcription .
0.9896 1.0000 1.0000 In lymphocytes , the octamer-binding protein Oct-2A and variants thereof are thought to contribute to the B-cell specific gene expression , while the ubiquitous protein proteinOct-1 seems to control general octamer site -dependent transcription .
In lymphocytes , the octamer-binding protein Oct-2A and variants thereof are thought to contribute to the DNAB-cell specific gene expression , while the ubiquitous protein Oct-1 seems to control general octamer site -dependent transcription .
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1.4698 10.9537 0.9999 Various other genes, for example interleukin-1 and MHC class II genes , contain an DNAoctamer sequence in the promoter and are expressed in cells of both the immune and nervous systems .
0.8775 1.0000 1.0000 Various other genes, for example interleukin-1 and MHC class II genes , contain an octamer sequence in the DNApromoter and are expressed in cells of both the immune and nervous systems .
4.1746 20.7324 10.8440 Various other genes, for example interleukin-1 and DNAMHC class II genes , contain an octamer sequence in the promoter and are expressed in cells of both the immune and nervous systems .
1.5404 10.0586 1.0000 Various other genes, for example proteininterleukin-1 and MHC class II genes , contain an octamer sequence in the promoter and are expressed in cells of both the immune and nervous systems .
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1.4985 10.9739 1.0000 This prompted us to analyze the proteinoctamer-binding proteins in the latter cells.
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3.5826 20.6162 10.8564 Using the electrophoretic mobility shift assay , at least six novel proteinoctamer binding proteins were detected in nuclear extracts of cultured mouse astrocytes .
3.3373 20.9723 10.7424 Using the electrophoretic mobility shift assay , at least six novel octamer binding proteins were detected in nuclear extracts of cell_linecultured mouse astrocytes .
0.6734 0.9999 0.9999 Using the electrophoretic mobility shift assay , at least six novel octamer binding proteins were detected in nuclear extracts of cultured mouse cell_typeastrocytes .
Using the electrophoretic mobility shift assay , at least six novel octamer binding proteins were detected in nuclear extracts of cell_typecultured mouse astrocytes .
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2.9939 10.8378 10.7455 These proteins are differentially expressed in human glioblastoma and cell_lineneuroblastoma cell lines .
1.3955 10.7987 0.9996 These proteins are differentially expressed in cell_linehuman glioblastoma and neuroblastoma cell lines .
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3.2900 20.9047 10.2597 The nervous system-derived (N-Oct) proteins bound to the DNAoctamer DNA sequence in a manner which is indistinguishable from the Oct-1 and Oct-2A proteins .
1.5471 10.3148 0.9981 The proteinnervous system-derived (N-Oct) proteins bound to the octamer DNA sequence in a manner which is indistinguishable from the Oct-1 and Oct-2A proteins .
1.4102 10.9422 1.0000 The nervous system-derived (N-Oct) proteins bound to the octamer DNA sequence in a manner which is indistinguishable from the proteinOct-1 and Oct-2A proteins .
1.4019 10.9688 0.9999 The nervous system-derived (N-Oct) proteins bound to the octamer DNA sequence in a manner which is indistinguishable from the Oct-1 and proteinOct-2A proteins .
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1.5419 10.8716 1.0000 The relationship of the proteinN-Oct proteins to Oct-1 and Oct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant Oct-1 and Oct-2A proteins.
0.9797 1.0000 1.0000 The relationship of the N-Oct proteins to Oct-1 and Oct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant proteinOct-1 and Oct-2A proteins.
0.9626 1.0000 1.0000 The relationship of the N-Oct proteins to Oct-1 and proteinOct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant Oct-1 and Oct-2A proteins.
0.8791 1.0000 1.0000 The relationship of the N-Oct proteins to proteinOct-1 and Oct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant Oct-1 and Oct-2A proteins.
1.3100 10.9470 0.9999 The relationship of the N-Oct proteins to Oct-1 and Oct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against proteinrecombinant Oct-1 and Oct-2A proteins.
The relationship of the N-Oct proteins to Oct-1 and Oct-2A was analyzed by proteolytic clipping bandshift assays and by their reactivity towards antisera raised against recombinant Oct-1 and proteinOct-2A proteins.
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1.3979 10.4724 1.0000 On the basis of these assays, all proteinN-Oct-factors were found to be distinct from the ubiquitous Oct-1 and the lymphoid-specific Oct-2A proteins.
1.2466 10.8645 0.9999 On the basis of these assays, all N-Oct-factors were found to be distinct from the proteinubiquitous Oct-1 and the lymphoid-specific Oct-2A proteins.
0.9579 1.0000 1.0000 On the basis of these assays, all N-Oct-factors were found to be distinct from the ubiquitous proteinOct-1 and the lymphoid-specific Oct-2A proteins.
0.9432 1.0000 0.9995 On the basis of these assays, all N-Oct-factors were found to be distinct from the ubiquitous Oct-1 and the lymphoid-specific proteinOct-2A proteins.
On the basis of these assays, all N-Oct-factors were found to be distinct from the ubiquitous Oct-1 and the proteinlymphoid-specific Oct-2A proteins.
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3.0052 20.4937 10.8961 In melanoma cells that contain the N-Oct-3 factor , a transfected lymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an DNAOct-2A expression vector .
2.1905 20.3459 1.0000 In melanoma cells that contain the proteinN-Oct-3 factor , a transfected lymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an Oct-2A expression vector .
1.5379 10.5261 0.9998 In cell_typemelanoma cells that contain the N-Oct-3 factor , a transfected lymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an Oct-2A expression vector .
1.4713 10.3336 0.9970 In melanoma cells that contain the N-Oct-3 factor , a transfected lymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an proteinOct-2A expression vector .
2.1425 20.0849 0.9999 In melanoma cells that contain the N-Oct-3 factor , a transfected DNAlymphocyte-specific promoter was neither activated nor was it repressed upon contransfection with an Oct-2A expression vector .
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1.7677 10.5091 1.0000 We therefore speculate that proteinN-Oct-3 and other N-Oct factors have a specific role in gene expression in cells of the nervous system .
1.6225 10.6284 1.0000 We therefore speculate that N-Oct-3 and other proteinN-Oct factors have a specific role in gene expression in cells of the nervous system .
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3.6015 30.2602 10.8239 Detection in non-erythroid cells of a factor with the binding characteristics of the proteinerythroid cell transcription factor EF1 .
1.9000 20.4452 0.9998 Detection in cell_typenon-erythroid cells of a factor with the binding characteristics of the erythroid cell transcription factor EF1 .
0.9633 0.9999 1.0000 Detection in non-erythroid cells of a factor with the binding characteristics of the erythroid cell transcription factor proteinEF1 .
1.2327 0.9997 10.3808 Detection in non-erythroid cells of a factor with the binding characteristics of the erythroid cell proteintranscription factor EF1 .
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2.9244 10.4086 10.5779 The proteinerythroid transcription factor erythroid factor-1 ( EF1 ) plays a critical role in the transcription of erythroid-specific genes .
2.0571 20.8029 0.9999 The erythroid transcription factor erythroid factor-1 ( EF1 ) plays a critical role in the transcription of DNAerythroid-specific genes .
0.9819 1.0000 1.0000 The erythroid transcription factor erythroid factor-1 ( proteinEF1 ) plays a critical role in the transcription of erythroid-specific genes .
0.8646 0.9966 0.9998 The erythroid transcription factor proteinerythroid factor-1 ( EF1 ) plays a critical role in the transcription of erythroid-specific genes .
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3.7759 20.8554 10.6445 Here we report the presence of a factor with the mobility and sequence-specific DNA-binding characteristics of EF1 at low abundance in a wide variety of cell_typenon-erythroid cell types .
1.6153 10.5447 1.0000 Here we report the presence of a factor with the mobility and sequence-specific DNA-binding characteristics of proteinEF1 at low abundance in a wide variety of non-erythroid cell types .
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2.4070 20.2749 1.0000 This is the first report of an EF1 -like activity in cell_typenon-erythroid cells and indicates that this factor may play a role in the regulation of genes expressed in such cells.
1.7363 10.1676 1.0000 This is the first report of an proteinEF1 -like activity in non-erythroid cells and indicates that this factor may play a role in the regulation of genes expressed in such cells.
1.5322 10.2171 1.0000 This is the first report of an EF1 -like activity in non-erythroid cells and indicates that this factor may play a role in the regulation of DNAgenes expressed in such cells.
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2.4521 20.0352 1.0000 Protein kinase inhibitor H-7 blocks accumulation of RNAunspliced mRNA of human T-cell leukemia virus type I ( HTLV-I ).
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4.3145 20.9153 10.5004 Rex , the post-transcriptional regulator of human T-cell leukemia virus type I ( HTLV-I ), is known to induce accumulation of the RNAunspliced viral gag-pol mRNA .
2.2395 20.6459 1.0000 Rex , the proteinpost-transcriptional regulator of human T-cell leukemia virus type I ( HTLV-I ), is known to induce accumulation of the unspliced viral gag-pol mRNA .
0.9431 1.0000 1.0000 proteinRex , the post-transcriptional regulator of human T-cell leukemia virus type I ( HTLV-I ), is known to induce accumulation of the unspliced viral gag-pol mRNA .
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1.8104 10.4607 1.0000 Rex is a proteinphosphoprotein found in the cell nucleolus , whose function may be regulated by its localization and phosphorylation .
0.9869 1.0000 1.0000 proteinRex is a phosphoprotein found in the cell nucleolus , whose function may be regulated by its localization and phosphorylation .
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1.7365 10.7662 1.0000 We have examined the role of phosphorylation on proteinRex function by using a protein kinase inhibitor , H-7 [ 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine ].
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5.5956 30.5101 20.9472 Treatment of an cell_lineHTLV-I infected human T-cell line with H-7 blocked specifically accumulation of the unspliced gag-pol mRNA , resulting in the decreased Gag protein synthesis that corresponds with the decreased in vivo phosphorylation of Rex .
4.2070 30.0508 10.6943 Treatment of an HTLV-I infected human T-cell line with H-7 blocked specifically accumulation of the RNAunspliced gag-pol mRNA , resulting in the decreased Gag protein synthesis that corresponds with the decreased in vivo phosphorylation of Rex .
2.1246 20.2087 1.0000 Treatment of an HTLV-I infected human T-cell line with H-7 blocked specifically accumulation of the unspliced gag-pol mRNA , resulting in the decreased Gag protein synthesis that corresponds with the decreased in vivo phosphorylation of proteinRex .
1.4133 10.7643 1.0000 Treatment of an HTLV-I infected human T-cell line with H-7 blocked specifically accumulation of the unspliced gag-pol mRNA , resulting in the decreased proteinGag protein synthesis that corresponds with the decreased in vivo phosphorylation of Rex .
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1.6309 10.5096 1.0000 Therefore, the phosphorylation of proteinRex is required for the viral RNA partition of HTLV-I .
1.6674 10.7847 1.0000 Therefore, the phosphorylation of Rex is required for the RNAviral RNA partition of HTLV-I .
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3.9963 20.4653 10.6521 Increased glucocorticoid responsiveness of cell_lineCD4+ T-cell clonal lines grown in serum-free media .
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5.0552 30.4660 20.6865 CEM-C7 , a cell_linehuman leukemic CD4+ T-lymphocyte cell line and three of its subclones, CEM-4R4 , CEM-3R43 , and ICR-27 , previously cultured in a medium supplemented with 5 to 10% fetal bovine serum , have been adapted to serum-free media .
1.7962 10.3998 1.0000 CEM-C7 , a human leukemic CD4+ T-lymphocyte cell line and three of its subclones, CEM-4R4 , CEM-3R43 , and cell_lineICR-27 , previously cultured in a medium supplemented with 5 to 10% fetal bovine serum , have been adapted to serum-free media .
0.9346 1.0000 1.0000 CEM-C7 , a human leukemic CD4+ T-lymphocyte cell line and three of its subclones, cell_lineCEM-4R4 , CEM-3R43 , and ICR-27 , previously cultured in a medium supplemented with 5 to 10% fetal bovine serum , have been adapted to serum-free media .
0.9136 1.0000 1.0000 CEM-C7 , a human leukemic CD4+ T-lymphocyte cell line and three of its subclones, CEM-4R4 , cell_lineCEM-3R43 , and ICR-27 , previously cultured in a medium supplemented with 5 to 10% fetal bovine serum , have been adapted to serum-free media .
0.8983 0.9999 1.0000 cell_lineCEM-C7 , a human leukemic CD4+ T-lymphocyte cell line and three of its subclones, CEM-4R4 , CEM-3R43 , and ICR-27 , previously cultured in a medium supplemented with 5 to 10% fetal bovine serum , have been adapted to serum-free media .
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3.9199 20.9830 10.8919 The best medium of those tested was RPMI 1640 supplemented with 5 micrograms/ml each transferrin and insulin + 5 ng/ml sodium selenite +/- 0.1% proteinbovine serum albumin .
0.9357 1.0000 1.0000 The best medium of those tested was RPMI 1640 supplemented with 5 micrograms/ml each transferrin and proteininsulin + 5 ng/ml sodium selenite +/- 0.1% bovine serum albumin .
0.8945 1.0000 1.0000 The best medium of those tested was RPMI 1640 supplemented with 5 micrograms/ml each proteintransferrin and insulin + 5 ng/ml sodium selenite +/- 0.1% bovine serum albumin .
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1.4901 10.9558 0.9999 While growing either with or without albumin, the several cell_lineclonal lines of CEM cells displayed growth similar to serum-supplemented cultures.
1.6069 10.6405 0.9998 While growing either with or without albumin, the several clonal lines of cell_lineCEM cells displayed growth similar to serum-supplemented cultures.
While growing either with or without albumin, the several clonal lines of cell_lineCEM cells displayed growth similar to serum-supplemented cultures.
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2.3129 20.3583 0.9999 Cell proliferation of cell_lineCEM-C7 cells cultured in both serum-free media has been sustained for 3 mo.
Cell proliferation of cell_lineCEM-C7 cells cultured in both serum-free media has been sustained for 3 mo.
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3.7538 20.7724 10.1666 The expression of CD4 , a marker for cell_typeT-derived lymphoid cells , was not significantly different in serum-free medium .
2.3788 20.2818 1.0000 The expression of proteinCD4 , a marker for T-derived lymphoid cells , was not significantly different in serum-free medium .
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2.1465 20.2109 1.0000 When grown in serum-free medium, CEM-C7 cells exhibited increased steroid responsiveness as evidenced by increased glucocorticoid receptor binding sites , increased induction of proteinglutamine synthetase , and cell lysis at lower concentrations of steroid .
1.8695 20.9374 0.9727 When grown in serum-free medium, CEM-C7 cells exhibited increased steroid responsiveness as evidenced by increased proteinglucocorticoid receptor binding sites , increased induction of glutamine synthetase , and cell lysis at lower concentrations of steroid .
3.9315 20.9660 10.8495 When grown in serum-free medium, CEM-C7 cells exhibited increased steroid responsiveness as evidenced by increased proteinglucocorticoid receptor binding sites , increased induction of glutamine synthetase , and cell lysis at lower concentrations of steroid .
1.6207 10.8582 0.9999 When grown in serum-free medium, cell_lineCEM-C7 cells exhibited increased steroid responsiveness as evidenced by increased glucocorticoid receptor binding sites , increased induction of glutamine synthetase , and cell lysis at lower concentrations of steroid .
When grown in serum-free medium, cell_lineCEM-C7 cells exhibited increased steroid responsiveness as evidenced by increased glucocorticoid receptor binding sites , increased induction of glutamine synthetase , and cell lysis at lower concentrations of steroid .
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1.8349 10.1331 1.0000 Receptor mutant subclones of cell_lineCEM-C7 , which are proven to be completely unresponsive to micromolar concentrations of dexamethasone when grown in serum-supplemented medium , become partially sensitive to the hormone after growth in defined medium.
1.6716 0.9963 10.1181 cell_lineReceptor mutant subclones of CEM-C7 , which are proven to be completely unresponsive to micromolar concentrations of dexamethasone when grown in serum-supplemented medium , become partially sensitive to the hormone after growth in defined medium.
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2.4440 20.3973 1.0000 The increased sensitivity of cell_lineCEM-C7 cells and its subclones to dexamethasone in serum-free medium returned to previous levels when these cells were recultured in serum-containing medium .
The increased sensitivity of cell_lineCEM-C7 cells and its subclones to dexamethasone in serum-free medium returned to previous levels when these cells were recultured in serum-containing medium .
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0.8859 0.9975 1.0000 [ proteinGlucocorticoid receptors on human peripheral mononuclear and polymorphonuclear leucocytes : changes in patients with yang-deficiency ]
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3.8233 20.0299 10.7197 It was found that, in former works, the glucocorticoid receptors ( GCR ) on cell_typeperipheral mixed leucocytes in patients with Yang-deficiency were decreased.
1.4958 10.9855 1.0000 It was found that, in former works, the proteinglucocorticoid receptors ( GCR ) on peripheral mixed leucocytes in patients with Yang-deficiency were decreased.
0.9533 1.0000 1.0000 It was found that, in former works, the glucocorticoid receptors ( proteinGCR ) on peripheral mixed leucocytes in patients with Yang-deficiency were decreased.
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2.1370 20.6770 0.9999 In this work, the cell_typemixed leucocytes were further separated into mononuclear (MNL) and polymorphonuclear (PML) leucocytes , and GCR were determined in each part of leucocytes .
1.5578 10.4377 0.9999 In this work, the mixed leucocytes were further separated into mononuclear (MNL) and polymorphonuclear (PML) leucocytes , and GCR were determined in each part of cell_typeleucocytes .
0.9323 1.0000 1.0000 In this work, the mixed leucocytes were further separated into mononuclear (MNL) and polymorphonuclear (PML) leucocytes , and proteinGCR were determined in each part of leucocytes .
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0.9614 1.0000 1.0000 GCR on MNL and cell_typePML in 6 Yang deficient patients were 3473 +/- 413 and 4433 +/- 651 sites/cell respectively, statistically significant from the normal control group (4462 +/- 962 and 5622 +/- 782 sites/cell respectively, P less than 0.05).
0.9465 1.0000 1.0000 proteinGCR on MNL and PML in 6 Yang deficient patients were 3473 +/- 413 and 4433 +/- 651 sites/cell respectively, statistically significant from the normal control group (4462 +/- 962 and 5622 +/- 782 sites/cell respectively, P less than 0.05).
0.9229 0.9999 1.0000 GCR on cell_typeMNL and PML in 6 Yang deficient patients were 3473 +/- 413 and 4433 +/- 651 sites/cell respectively, statistically significant from the normal control group (4462 +/- 962 and 5622 +/- 782 sites/cell respectively, P less than 0.05).
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1.6035 10.3371 0.9999 GCR on MNL , PML and cell_typemixed leucocytes in 5 patients were determined simultaneously, and all lowered from the control group .
0.9588 1.0000 1.0000 proteinGCR on MNL , PML and mixed leucocytes in 5 patients were determined simultaneously, and all lowered from the control group .
0.9368 1.0000 1.0000 GCR on MNL , cell_typePML and mixed leucocytes in 5 patients were determined simultaneously, and all lowered from the control group .
0.9120 0.9998 1.0000 GCR on cell_typeMNL , PML and mixed leucocytes in 5 patients were determined simultaneously, and all lowered from the control group .
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1.7482 10.1443 1.0000 The results were 3369 +/- 370, 4986 +/- 419 and 4524 +/- 852 sites/cell respectively, with the lowest proteinGCR on MNL and highest on PML .
1.6913 10.4425 1.0000 The results were 3369 +/- 370, 4986 +/- 419 and 4524 +/- 852 sites/cell respectively, with the lowest GCR on MNL and highest on cell_typePML .
0.8933 0.9999 1.0000 The results were 3369 +/- 370, 4986 +/- 419 and 4524 +/- 852 sites/cell respectively, with the lowest GCR on cell_typeMNL and highest on PML .
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2.8713 10.7801 10.9827 The proteinubiquitous octamer-binding protein (s) is sufficient for transcription of immunoglobulin genes .
1.9270 20.5474 0.9999 The ubiquitous octamer-binding protein (s) is sufficient for transcription of DNAimmunoglobulin genes .
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3.8380 20.5879 10.4713 All immunoglobulin genes contain a conserved DNAoctanucleotide promoter element , ATGCAAAT , which has been shown to be required for their normal B-cell-specific transcription .
1.5326 10.9768 0.9999 All DNAimmunoglobulin genes contain a conserved octanucleotide promoter element , ATGCAAAT , which has been shown to be required for their normal B-cell-specific transcription .
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1.6427 10.4809 1.0000 Proteins that bind this octamer have been purified, and DNAcDNAs encoding octamer-binding proteins have been cloned.
1.5900 10.7989 1.0000 Proteins that bind this octamer have been purified, and cDNAs encoding proteinoctamer-binding proteins have been cloned.
1.6660 10.3388 1.0000 Proteins that bind this DNAoctamer have been purified, and cDNAs encoding octamer-binding proteins have been cloned.
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1.7401 10.1938 1.0000 Some of these proteins (referred to as proteinOTF-2 ) are lymphoid specific, whereas at least one other, and possibly more (referred to as OTF-1 ), is found ubiquitously in all cell types.
1.7243 10.3268 1.0000 Some of these proteins (referred to as OTF-2 ) are lymphoid specific, whereas at least one other, and possibly more (referred to as proteinOTF-1 ), is found ubiquitously in all cell types.
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2.3897 20.5404 1.0000 The exact role of these different proteins in directing the tissue-specific expression of DNAimmunoglobulin genes is unclear.
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3.8480 20.5027 10.8860 We have identified two cell_linehuman pre-B-cell lines that contain extremely low levels of OTF-2 yet still express high levels of steady-state immunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an immunoglobulin gene in vitro.
2.0880 20.4339 1.0000 We have identified two human pre-B-cell lines that contain extremely low levels of OTF-2 yet still express high levels of steady-state immunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an DNAimmunoglobulin gene in vitro.
1.4354 20.1944 0.8311 We have identified two human pre-B-cell lines that contain extremely low levels of OTF-2 yet still express high levels of steady-state proteinimmunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an immunoglobulin gene in vitro.
0.8498 1.0000 1.0000 We have identified two human pre-B-cell lines that contain extremely low levels of proteinOTF-2 yet still express high levels of steady-state immunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an immunoglobulin gene in vitro.
2.6485 20.0047 0.9998 We have identified two human pre-B-cell lines that contain extremely low levels of OTF-2 yet still express high levels of steady-state RNAimmunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an immunoglobulin gene in vitro.
We have identified two human pre-B-cell lines that contain extremely low levels of OTF-2 yet still express high levels of RNAsteady-state immunoglobulin heavy-chain mRNA in vivo and efficiently transcribe an immunoglobulin gene in vitro.
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2.1717 20.5976 0.9999 Addition of a highly enriched preparation of OTF-1 made from one of these pre-B cells or from HeLa cells specifically stimulated in vitro transcription of an DNAimmunoglobulin gene .
1.6121 10.8997 1.0000 Addition of a highly enriched preparation of proteinOTF-1 made from one of these pre-B cells or from HeLa cells specifically stimulated in vitro transcription of an immunoglobulin gene .
1.5887 10.7674 0.9999 Addition of a highly enriched preparation of OTF-1 made from one of these pre-B cells or from cell_lineHeLa cells specifically stimulated in vitro transcription of an immunoglobulin gene .
2.3212 20.2762 0.9999 Addition of a highly enriched preparation of OTF-1 made from one of these cell_typepre-B cells or from HeLa cells specifically stimulated in vitro transcription of an immunoglobulin gene .
Addition of a highly enriched preparation of OTF-1 made from one of these cell_linepre-B cells or from HeLa cells specifically stimulated in vitro transcription of an immunoglobulin gene .
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1.6306 10.7051 1.0000 Furthermore, OFT-1 appeared to have approximately the same transactivation ability as proteinOTF-2 when normalized for binding activity.
0.9317 1.0000 1.0000 Furthermore, proteinOFT-1 appeared to have approximately the same transactivation ability as OTF-2 when normalized for binding activity.
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2.2759 20.1043 1.0000 These results suggest that OTF-1 , without OTF-2 , is sufficient for transcription of DNAimmunoglobulin genes and that OTF-2 alone is not responsible for the B-cell-specific regulation of immunoglobulin gene expression .
2.2499 20.1758 0.9997 These results suggest that OTF-1 , without OTF-2 , is sufficient for transcription of immunoglobulin genes and that OTF-2 alone is not responsible for the B-cell-specific regulation of DNAimmunoglobulin gene expression .
1.6923 10.1295 1.0000 These results suggest that proteinOTF-1 , without OTF-2 , is sufficient for transcription of immunoglobulin genes and that OTF-2 alone is not responsible for the B-cell-specific regulation of immunoglobulin gene expression .
1.6572 10.4398 1.0000 These results suggest that OTF-1 , without proteinOTF-2 , is sufficient for transcription of immunoglobulin genes and that OTF-2 alone is not responsible for the B-cell-specific regulation of immunoglobulin gene expression .
0.8573 1.0000 1.0000 These results suggest that OTF-1 , without OTF-2 , is sufficient for transcription of immunoglobulin genes and that proteinOTF-2 alone is not responsible for the B-cell-specific regulation of immunoglobulin gene expression .
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3.1095 10.7598 10.2812 In vitro binding of aldosterone to mineralocorticoid receptors on cell_typehuman mononuclear leukocytes ( HML ) and its effects on the intracellular sodium and potassium concentrations of HML have already been described.
1.6186 10.7244 1.0000 In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes ( HML ) and its effects on the intracellular sodium and potassium concentrations of cell_typeHML have already been described.
1.5253 10.9089 0.9999 In vitro binding of aldosterone to proteinmineralocorticoid receptors on human mononuclear leukocytes ( HML ) and its effects on the intracellular sodium and potassium concentrations of HML have already been described.
0.9420 1.0000 1.0000 In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes ( cell_typeHML ) and its effects on the intracellular sodium and potassium concentrations of HML have already been described.
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0.8285 10.6575 1.0000 In only four patients sodium in cell_typeHML without incubation was elevated compared with the range for normal persons .
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0.9711 1.0000 1.0000 Plasma proteinrenin activity and aldosterone were not correlated with the electrolyte response and were within the normal limits.
proteinPlasma renin activity and aldosterone were not correlated with the electrolyte response and were within the normal limits.
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2.4279 20.7331 0.9988 The number of proteinmineralocorticoid receptors /cell were within or close to the normal range (n = 9).
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2.4406 20.5722 1.0000 The independence of intracellular electrolytes from aldosterone despite a normal number of proteinmineralocorticoid receptors may reflect an impairment of the mineralocorticoid effector mechanism in the HML of patients with essential hypertension .
1.7555 10.2281 1.0000 The independence of intracellular electrolytes from aldosterone despite a normal number of mineralocorticoid receptors may reflect an impairment of the mineralocorticoid effector mechanism in the cell_typeHML of patients with essential hypertension .
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1.7164 10.4515 1.0000 [Differential diagnostic value of receptors of 1,25-dihydroxyvitamin D3 ( calcitriol ) determination in cell_typelymphocytes of children with rickets and rickets -like diseases ]
1.6704 10.8869 1.0000 [Differential diagnostic value of proteinreceptors of 1,25-dihydroxyvitamin D3 ( calcitriol ) determination in lymphocytes of children with rickets and rickets -like diseases ]
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1.7456 10.2588 1.0000 The authors provide the results of studying 1,25-dihydroxyvitamin D3 ( calcitriol ) in cell_typelymphocytes of children with rickets and rickets -like diseases .
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3.9209 20.3770 10.4560 Alteration of gene transcription by inhibition of specific proteintranscriptional regulatory proteins is necessary for determining how these factors participate in cellular differentiation .
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4.2414 20.5259 10.7746 Inhibition of proteinsequence-specific DNA-binding proteins was achieved with double-stranded (ds) phosphorothioate oligonucleotides that contained octamer or kappa B consensus sequences .
3.7230 20.3682 10.8310 Inhibition of sequence-specific DNA-binding proteins was achieved with double-stranded (ds) phosphorothioate oligonucleotides that contained octamer or DNAkappa B consensus sequences .
1.3934 10.2368 1.0000 Inhibition of sequence-specific DNA-binding proteins was achieved with double-stranded (ds) phosphorothioate oligonucleotides that contained DNAoctamer or kappa B consensus sequences .
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3.6250 20.0815 10.4351 The phosphorothioate oligonucleotides specifically bound either proteinoctamer transcription factor or nuclear factor (NF)-kappa B .
3.0938 10.9721 10.7137 The phosphorothioate oligonucleotides specifically bound either octamer transcription factor or proteinnuclear factor (NF)-kappa B .
1.3714 0.9998 10.0381 The phosphorothioate oligonucleotides specifically bound either octamer proteintranscription factor or nuclear factor (NF)-kappa B .
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6.1753 30.8142 10.8349 Octamer-dependent activation of a reporter plasmid or NF-kappa B -dependent activation of the DNAhuman immunodeficiency virus ( HIV ) enhancer was inhibited when the appropriate phosphorothioate oligonucleotide was added to a transiently transfected B cell line .
5.4499 30.7721 20.9781 Octamer-dependent activation of a reporter plasmid or NF-kappa B -dependent activation of the human immunodeficiency virus ( HIV ) enhancer was inhibited when the appropriate phosphorothioate oligonucleotide was added to a cell_linetransiently transfected B cell line .
1.7616 20.7681 0.9999 Octamer-dependent activation of a DNAreporter plasmid or NF-kappa B -dependent activation of the human immunodeficiency virus ( HIV ) enhancer was inhibited when the appropriate phosphorothioate oligonucleotide was added to a transiently transfected B cell line .
1.4548 10.6359 1.0000 Octamer-dependent activation of a reporter plasmid or proteinNF-kappa B -dependent activation of the human immunodeficiency virus ( HIV ) enhancer was inhibited when the appropriate phosphorothioate oligonucleotide was added to a transiently transfected B cell line .
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3.5563 20.9378 10.8349 Addition of phosphorothioate oligonucleotides that contained the octamer consensus to Jurkat T leukemia cells inhibited interleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a DNAmutated octamer site in the IL-2 enhancer .
3.1922 10.5137 10.8435 Addition of phosphorothioate oligonucleotides that contained the octamer consensus to cell_lineJurkat T leukemia cells inhibited interleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the IL-2 enhancer .
2.1398 20.5647 0.9999 Addition of phosphorothioate oligonucleotides that contained the octamer consensus to Jurkat T leukemia cells inhibited interleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the DNAIL-2 enhancer .
1.9569 20.4087 0.9997 Addition of phosphorothioate oligonucleotides that contained the DNAoctamer consensus to Jurkat T leukemia cells inhibited interleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the IL-2 enhancer .
0.9804 1.0000 1.0000 Addition of phosphorothioate oligonucleotides that contained the octamer consensus to Jurkat T leukemia cells inhibited interleukin-2 ( proteinIL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the IL-2 enhancer .
0.9715 1.0000 1.0000 Addition of phosphorothioate oligonucleotides that contained the octamer consensus to Jurkat T leukemia cells inhibited proteininterleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the IL-2 enhancer .
1.5313 20.8856 0.9785 Addition of phosphorothioate oligonucleotides that contained the octamer consensus to Jurkat T leukemia cells inhibited interleukin-2 ( IL-2 ) secretion to a degree similar to that observed with a mutated octamer site in the proteinIL-2 enhancer .
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1.6408 10.9568 1.0000 The ds phosphorothioate oligonucleotides probably compete for binding of specific proteintranscription factors and may provide anti-viral , immunosuppressive , or other therapeutic effects .
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1.6163 10.8672 1.0000 [Effect of the regimen of kidney-tonifying and qi-invigorating on aging changes of proteinglucocorticoid receptor ]
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2.3396 20.5166 1.0000 The plasma cortisol concentration and the sites of proteinglucocorticoid receptor ( GCR ) in the peripheral lymphocytes were measured in 32 healthy aged persons and 13 young adults .
1.6136 10.9528 0.9999 The plasma cortisol concentration and the sites of glucocorticoid receptor ( GCR ) in the cell_typeperipheral lymphocytes were measured in 32 healthy aged persons and 13 young adults .
0.9711 1.0000 1.0000 The plasma cortisol concentration and the sites of glucocorticoid receptor ( proteinGCR ) in the peripheral lymphocytes were measured in 32 healthy aged persons and 13 young adults .
The plasma cortisol concentration and the sites of glucocorticoid receptor ( GCR ) in the peripheral cell_typelymphocytes were measured in 32 healthy aged persons and 13 young adults .
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3.0255 20.7828 10.7537 In animal experiment , GCR of cell_typespleen lymphocytic cell was also measured in 18 aged rats and 9 young rats .
1.5466 10.9824 1.0000 In animal experiment , proteinGCR of spleen lymphocytic cell was also measured in 18 aged rats and 9 young rats .
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1.7804 10.6459 1.0000 The results showed that proteinGCR was significantly lower in the aged persons or rats than that in the young while the plasma cortisol level didn't change with aging.
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1.7490 10.5715 1.0000 So we think that proteinGCR is more sensitive than the plasma cortisol level to reflect the aging change of the adrenal cortex function .
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1.8133 10.3469 1.0000 After the treatment with the regimen of Kidney-tonifying and Qi-invigorating , the proteinGCR of the aged persons and rats was enhanced, and in this way, the function of the aged adrenal cortex was improved.
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1.6214 10.9834 1.0000 Interferon affects proteinnuclear proteins in cells of clinically sensitive chronic myelogenous leukemia patients .
0.9608 1.0000 1.0000 proteinInterferon affects nuclear proteins in cells of clinically sensitive chronic myelogenous leukemia patients .
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1.9981 20.3306 0.9999 Cytoplasmic protein extracts from chronic myelogenous leukemia ( CML ) cells contained an activity that altered the electrophoretic mobility of complexes formed between proteinnuclear proteins and the transcriptional enhancers of interferon (IFN)-inducible genes.
5.8710 30.2593 20.6475 Cytoplasmic protein extracts from cell_linechronic myelogenous leukemia ( CML ) cells contained an activity that altered the electrophoretic mobility of complexes formed between nuclear proteins and the transcriptional enhancers of interferon (IFN)-inducible genes.
1.2977 10.4894 0.9997 Cytoplasmic protein extracts from chronic myelogenous leukemia ( CML ) cells contained an activity that altered the electrophoretic mobility of complexes formed between nuclear proteins and the DNAtranscriptional enhancers of interferon (IFN)-inducible genes.
Cytoplasmic protein extracts from cell_typechronic myelogenous leukemia ( CML ) cells contained an activity that altered the electrophoretic mobility of complexes formed between nuclear proteins and the transcriptional enhancers of interferon (IFN)-inducible genes.
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3.4914 20.3707 10.6499 Exposure of CML cells to IFN-alpha diminished the effect of the proteinCML cytoplasmic proteins on these nuclear protein-DNA complexes .
3.3658 20.3514 10.8826 Exposure of CML cells to IFN-alpha diminished the effect of the CML cytoplasmic proteins on these proteinnuclear protein-DNA complexes .
0.8467 1.0000 1.0000 Exposure of CML cells to proteinIFN-alpha diminished the effect of the CML cytoplasmic proteins on these nuclear protein-DNA complexes .
2.1195 20.1818 0.9999 Exposure of cell_lineCML cells to IFN-alpha diminished the effect of the CML cytoplasmic proteins on these nuclear protein-DNA complexes .
0.6766 0.9997 0.9998 Exposure of CML cells to IFN-alpha diminished the effect of the CML proteincytoplasmic proteins on these nuclear protein-DNA complexes .
Exposure of cell_typeCML cells to IFN-alpha diminished the effect of the CML cytoplasmic proteins on these nuclear protein-DNA complexes .
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3.7349 20.8293 10.4580 The presence of clinical responsiveness to IFN-alpha correlated with the sensitivity to the IFN -induced change in the electrophoretic mobility of proteinnuclear protein-DNA complexes .
1.5692 10.7372 1.0000 The presence of clinical responsiveness to proteinIFN-alpha correlated with the sensitivity to the IFN -induced change in the electrophoretic mobility of nuclear protein-DNA complexes .
0.9130 1.0000 1.0000 The presence of clinical responsiveness to IFN-alpha correlated with the sensitivity to the proteinIFN -induced change in the electrophoretic mobility of nuclear protein-DNA complexes .
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2.4045 20.3622 1.0000 These data suggest that the action of IFN-alpha in CML may be linked to a pathway that can result in posttranslational modification of proteinnuclear proteins .
1.6994 10.6258 1.0000 These data suggest that the action of proteinIFN-alpha in CML may be linked to a pathway that can result in posttranslational modification of nuclear proteins .
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2.3721 20.6883 10.3524 Epstein-Barr virus nuclear antigen 2 transactivates proteinlatent membrane protein LMP1 .
2.3152 0.9992 20.2643 proteinEpstein-Barr virus nuclear antigen 2 transactivates latent membrane protein LMP1 .
0.9771 1.0000 0.9999 Epstein-Barr virus nuclear antigen 2 transactivates latent membrane protein proteinLMP1 .
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6.3265 30.8928 20.0481 Several lines of evidence are compatible with the hypothesis that proteinEpstein-Barr virus ( EBV ) nuclear antigen 2 ( EBNA-2 ) or leader protein ( EBNA-LP ) affects expression of the EBV latent infection membrane protein LMP1 .
4.2990 40.8119 20.3696 Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus ( EBV ) nuclear antigen 2 ( EBNA-2 ) or leader protein ( EBNA-LP ) affects expression of the proteinEBV latent infection membrane protein LMP1 .
1.2813 10.9973 1.0000 Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus ( EBV ) nuclear antigen 2 ( EBNA-2 ) or proteinleader protein ( EBNA-LP ) affects expression of the EBV latent infection membrane protein LMP1 .
0.9649 1.0000 1.0000 Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus ( EBV ) nuclear antigen 2 ( proteinEBNA-2 ) or leader protein ( EBNA-LP ) affects expression of the EBV latent infection membrane protein LMP1 .
0.9487 0.9996 0.9999 Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus ( EBV ) nuclear antigen 2 ( EBNA-2 ) or leader protein ( EBNA-LP ) affects expression of the EBV latent infection membrane protein proteinLMP1 .
0.9258 1.0000 1.0000 Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus ( EBV ) nuclear antigen 2 ( EBNA-2 ) or leader protein ( proteinEBNA-LP ) affects expression of the EBV latent infection membrane protein LMP1 .
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5.5168 30.5931 10.7709 (i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in cell_lineP3HR-1-infected Burkitt's lymphoma cells and the P3HR-1 or Daudi cell line .
1.5947 10.2939 1.0000 (i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased proteinLMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the P3HR-1 or Daudi cell line .
1.4828 10.5728 1.0000 (i) Acute transfection and expression of proteinEBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the P3HR-1 or Daudi cell line .
1.4005 20.8606 0.9994 (i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the P3HR-1 or cell_lineDaudi cell line .
0.7855 0.9999 1.0000 (i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the proteinP3HR-1 or Daudi cell line .
(i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the cell_lineP3HR-1 or Daudi cell line .
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1.6051 10.5955 1.0000 (ii) Transfection and expression of EBNA-LP alone had no effect on proteinLMP1 expression and did not act synergistically with EBNA-2 to affect LMP1 expression .
1.6025 10.4854 1.0000 (ii) Transfection and expression of EBNA-LP alone had no effect on LMP1 expression and did not act synergistically with proteinEBNA-2 to affect LMP1 expression .
1.5653 10.8852 1.0000 (ii) Transfection and expression of EBNA-LP alone had no effect on LMP1 expression and did not act synergistically with EBNA-2 to affect proteinLMP1 expression .
1.5574 10.7753 1.0000 (ii) Transfection and expression of proteinEBNA-LP alone had no effect on LMP1 expression and did not act synergistically with EBNA-2 to affect LMP1 expression .
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1.5497 10.5299 1.0000 (iii) LMP1 expression in cell_lineDaudi and P3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in Daudi cells increased LMP1 mRNA .
1.5390 10.8381 0.9998 (iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in Daudi cells increased RNALMP1 mRNA .
1.4201 10.3520 0.9998 (iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in cell_lineDaudi cells increased LMP1 mRNA .
1.3062 10.1975 0.9819 (iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in Daudi cells increased proteinLMP1 mRNA .
1.2150 10.9466 0.9997 (iii) LMP1 expression in Daudi and cell_lineP3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in Daudi cells increased LMP1 mRNA .
0.9612 1.0000 1.0000 (iii) proteinLMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level , and EBNA-2 expression in Daudi cells increased LMP1 mRNA .
0.8889 0.9999 1.0000 (iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level , and proteinEBNA-2 expression in Daudi cells increased LMP1 mRNA .
(iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the RNAmRNA level , and EBNA-2 expression in Daudi cells increased LMP1 mRNA .
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4.1732 20.9304 10.8221 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of DNArecombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
3.7142 20.3727 10.9935 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the cell_lineEBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
1.7530 20.5047 0.9999 (iv) No other DNAEBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
1.6597 10.2067 1.0000 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and cell_lineBL30 .
1.4079 10.6719 1.0000 (iv) No other EBV genes were required for EBNA-2 transactivation of proteinLMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
0.9587 1.0000 1.0000 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced proteinLMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
0.9416 0.9999 1.0000 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines cell_lineBJAB , Louckes , and BL30 .
0.9127 1.0000 1.0000 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , cell_lineLouckes , and BL30 .
0.9127 1.0000 0.9885 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant proteinEBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
0.9076 1.0000 0.9941 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic proteinLMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
0.7905 1.0000 1.0000 (iv) No other EBV genes were required for proteinEBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
3.7267 20.6623 10.5273 (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and DNAgenomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
(iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic DNALMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB , Louckes , and BL30 .
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3.8291 20.9330 10.7857 (v) An EBNA-2 -responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a DNAchloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
2.8572 20.9038 10.8052 (v) An EBNA-2 -responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an DNAEBNA-2 expression vector .
2.1997 20.6378 10.9972 (v) An DNAEBNA-2 -responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
2.1458 20.3352 0.9999 (v) An EBNA-2 -responsive element was found within the -512 to +40 DNALMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
2.1322 20.1102 0.9905 (v) An EBNA-2 -responsive element was found within the -512 to +40 proteinLMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
1.9650 20.5851 0.9952 (v) An EBNA-2 -responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an proteinEBNA-2 expression vector .
1.4797 10.6776 0.9973 (v) An proteinEBNA-2 -responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
(v) An EBNA-2 -responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a proteinchloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
(v) An EBNA-2 -responsive element was found within the DNA-512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector .
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3.4065 20.7978 10.7246 (vi) The EBV type 2 EBNA-2 transactivated LMP1 as well as the proteinEBV type 1 EBNA-2 .
0.9203 0.9999 1.0000 (vi) The EBV type 2 proteinEBNA-2 transactivated LMP1 as well as the EBV type 1 EBNA-2 .
0.9091 0.9999 1.0000 (vi) The EBV type 2 EBNA-2 transactivated LMP1 as well as the EBV type 1 proteinEBNA-2 .
0.8576 0.9999 1.0000 (vi) The EBV type 2 EBNA-2 transactivated proteinLMP1 as well as the EBV type 1 EBNA-2 .
3.5017 20.6627 10.8287 (vi) The proteinEBV type 2 EBNA-2 transactivated LMP1 as well as the EBV type 1 EBNA-2 .
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1.9224 20.3683 0.9922 (vii) Two deletions within the proteinEBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a transformation-competent EBNA-2 deletion mutant did transactivate LMP1 .
1.5079 10.3640 1.0000 (vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate proteinLMP1 , whereas a transformation-competent EBNA-2 deletion mutant did transactivate LMP1 .
1.4399 10.2011 1.0000 (vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a transformation-competent EBNA-2 deletion mutant did transactivate proteinLMP1 .
0.9251 1.0000 0.9969 (vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a transformation-competent proteinEBNA-2 deletion mutant did transactivate LMP1 .
4.6416 20.9000 10.9170 (vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a proteintransformation-competent EBNA-2 deletion mutant did transactivate LMP1 .
2.0209 20.3385 1.0000 (vii) Two deletions within the DNAEBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a transformation-competent EBNA-2 deletion mutant did transactivate LMP1 .
(vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1 , whereas a DNAtransformation-competent EBNA-2 deletion mutant did transactivate LMP1 .
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1.6346 10.1351 1.0000 LMP1 is a potent effector of B-lymphocyte activation and can act synergistically with proteinEBNA-2 to induce cellular CD23 gene expression .
0.9749 1.0000 1.0000 proteinLMP1 is a potent effector of B-lymphocyte activation and can act synergistically with EBNA-2 to induce cellular CD23 gene expression .
2.2486 20.7535 0.9999 LMP1 is a potent effector of B-lymphocyte activation and can act synergistically with EBNA-2 to induce cellular DNACD23 gene expression .
1.6237 10.0759 1.0000 LMP1 is a potent effector of cell_typeB-lymphocyte activation and can act synergistically with EBNA-2 to induce cellular CD23 gene expression .
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1.6902 10.3920 1.0000 Thus, EBNA-2 transactivation of proteinLMP1 amplifies the biological impact of EBNA-2 and underscores its central role in EBV-induced growth transformation .
1.6846 10.2686 1.0000 Thus, EBNA-2 transactivation of LMP1 amplifies the biological impact of proteinEBNA-2 and underscores its central role in EBV-induced growth transformation .
0.9102 0.9999 1.0000 Thus, proteinEBNA-2 transactivation of LMP1 amplifies the biological impact of EBNA-2 and underscores its central role in EBV-induced growth transformation .
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2.0285 20.8262 10.1091 The expression of c-fos , c-jun , and c-myc genes is regulated by heat shock in cell_typehuman lymphoid cells .
The expression of DNAc-fos , c-jun , and c-myc genes is regulated by heat shock in human lymphoid cells .
The expression of c-fos , DNAc-jun , and c-myc genes is regulated by heat shock in human lymphoid cells .
The expression of c-fos , c-jun , and DNAc-myc genes is regulated by heat shock in human lymphoid cells .
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2.0712 20.7336 0.9994 The effect of heat shock on the expression of the DNAnuclear protooncogenes c-fos , c-jun , and c-myc was studied in human lymphoid cells .
2.0471 20.3789 10.8111 The effect of heat shock on the expression of the nuclear protooncogenes c-fos , c-jun , and c-myc was studied in cell_typehuman lymphoid cells .
1.7305 10.9901 1.0000 The effect of heat shock on the expression of the nuclear protooncogenes c-fos , c-jun , and DNAc-myc was studied in human lymphoid cells .
0.9423 1.0000 1.0000 The effect of heat shock on the expression of the nuclear protooncogenes c-fos , DNAc-jun , and c-myc was studied in human lymphoid cells .
0.8734 1.0000 0.9999 The effect of heat shock on the expression of the nuclear protooncogenes DNAc-fos , c-jun , and c-myc was studied in human lymphoid cells .
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1.6338 10.8212 0.9999 Heat shock caused an increase in c-fos and c-jun mRNA levels and a decrease in RNAc-myc mRNA levels in pre-B (Hyon) and T (DND-41) cell lines as well as in freshly isolated normal human thymocytes.
Heat shock caused an increase in c-fos and c-jun mRNA levels and a decrease in DNAc-myc mRNA levels in pre-B (Hyon) and T (DND-41) cell lines as well as in freshly isolated normal human thymocytes.
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1.7742 10.6157 1.0000 The changes in the mRNA levels of these DNAprotooncogenes in Hyon cells were most pronounced at 42 and 43 degrees C; kinetic analysis demonstrated that the changes could be detected within 30 min of heat shock .
1.5044 10.6893 0.9999 The changes in the mRNA levels of these protooncogenes in cell_lineHyon cells were most pronounced at 42 and 43 degrees C; kinetic analysis demonstrated that the changes could be detected within 30 min of heat shock .
1.1506 10.0570 1.0000 The changes in the RNAmRNA levels of these protooncogenes in Hyon cells were most pronounced at 42 and 43 degrees C; kinetic analysis demonstrated that the changes could be detected within 30 min of heat shock .
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1.5483 10.0810 0.9999 Altered transcription of c-fos and DNAc-myc genes was the primary effect of heat shock .
1.5184 10.8407 1.0000 Altered transcription of DNAc-fos and c-myc genes was the primary effect of heat shock .
Altered transcription of c-fos and DNAc-myc genes was the primary effect of heat shock .
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1.7068 10.8694 1.0000 Secondarily, heat shock of Hyon cells stabilized the RNAc-myc mRNA level by increasing its half-life from 24 to 45 min.
1.5646 10.7832 0.9999 Secondarily, heat shock of cell_typeHyon cells stabilized the c-myc mRNA level by increasing its half-life from 24 to 45 min.
Secondarily, heat shock of cell_lineHyon cells stabilized the c-myc mRNA level by increasing its half-life from 24 to 45 min.
Secondarily, heat shock of Hyon cells stabilized the DNAc-myc mRNA level by increasing its half-life from 24 to 45 min.
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1.7510 10.9744 1.0000 The overall effect of heat shock on RNAc-myc mRNA level , however, was a marked inhibition of its transcription .
The overall effect of heat shock on DNAc-myc mRNA level , however, was a marked inhibition of its transcription .
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2.3275 20.2615 1.0000 These results demonstrate that the transcription of DNAnuclear protooncogenes is regulated by heat shock indicating a role for nuclear protooncogenes in the stress response of lymphoid cells .
2.1539 20.4041 1.0000 These results demonstrate that the transcription of nuclear protooncogenes is regulated by heat shock indicating a role for DNAnuclear protooncogenes in the stress response of lymphoid cells .
1.5099 10.9503 0.9997 These results demonstrate that the transcription of nuclear protooncogenes is regulated by heat shock indicating a role for nuclear protooncogenes in the stress response of cell_typelymphoid cells .
0.8530 1.0000 1.0000 These results demonstrate that the transcription of nuclear protooncogenes is regulated by heat shock indicating a role for nuclear DNAprotooncogenes in the stress response of lymphoid cells .
These results demonstrate that the transcription of nuclear DNAprotooncogenes is regulated by heat shock indicating a role for nuclear protooncogenes in the stress response of lymphoid cells .
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5.7782 30.6678 20.9796 Mapping of B-cell epitopes of the proteinhuman hepatitis B virus X protein .
1.5429 20.4316 0.9997 Mapping of proteinB-cell epitopes of the human hepatitis B virus X protein .
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3.8320 20.7192 10.6109 The immune response to the X protein of human hepatitis B virus ( HBV ) was studied by epitope mapping by using a set of proteinMS2-HBx fusion proteins and synthetic peptides .
2.2115 20.8072 1.0000 The immune response to the proteinX protein of human hepatitis B virus ( HBV ) was studied by epitope mapping by using a set of MS2-HBx fusion proteins and synthetic peptides .
0.8866 1.0000 1.0000 The immune response to the X protein of human hepatitis B virus ( HBV ) was studied by proteinepitope mapping by using a set of MS2-HBx fusion proteins and synthetic peptides .
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0.5435 0.9999 1.0000 proteinAntibodies in sera of patients with acute and chronic HBV infection showed a multispecific immune response .
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1.7580 10.4502 1.0000 Each serum contained proteinantibodies to a different set of epitopes , which taken together cover most of the HBx sequence .
1.7415 10.1500 1.0000 Each serum contained antibodies to a different set of proteinepitopes , which taken together cover most of the HBx sequence .
2.3623 20.3870 1.0000 Each serum contained antibodies to a different set of epitopes , which taken together cover most of the DNAHBx sequence .
Each serum contained antibodies to a different set of epitopes , which taken together cover most of the proteinHBx sequence .
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1.6894 10.8518 1.0000 Some of the epitopes were detectable only by immunoblotting with proteinfusion proteins ; others were detectable only by an enzyme-linked immunosorbent assay ( ELISA ) with synthetic peptides .
1.8383 10.0068 1.0000 Some of the proteinepitopes were detectable only by immunoblotting with fusion proteins ; others were detectable only by an enzyme-linked immunosorbent assay ( ELISA ) with synthetic peptides .
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3.6163 20.9699 10.9927 The carboxy-terminal half of the HBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short proteinimmunodominant antigenic region with at least two major nonoverlapping epitopes .
2.2785 20.2436 1.0000 The carboxy-terminal half of the proteinHBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major nonoverlapping epitopes .
1.6139 10.1510 1.0000 The carboxy-terminal half of the HBx protein was preferentially recognized by proteinantibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major nonoverlapping epitopes .
1.5197 10.7674 0.9999 The proteincarboxy-terminal half of the HBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major nonoverlapping epitopes .
3.5361 20.9065 10.8515 The carboxy-terminal half of the HBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two proteinmajor nonoverlapping epitopes .
0.5447 1.0000 1.0000 The carboxy-terminal half of the HBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major nonoverlapping proteinepitopes .
The carboxy-terminal half of the HBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major proteinnonoverlapping epitopes .
The carboxy-terminal half of the proteinHBx protein was preferentially recognized by antibodies from patients with chronic hepatitis and contained a short immunodominant antigenic region with at least two major nonoverlapping epitopes .
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0.6895 1.0000 0.9998 Anti- proteinHBx antibody titers as revealed by peptide ELISAs were highest and most frequent in patients with chronic hepatitis and usually low in acutely infected patients and asymptomatic carriers .
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1.7759 10.3336 1.0000 The data demonstrate a remarkable qualitative and quantitative heterogeneity of the humoral proteinHBx immune response which can be monitored by HBx -specific peptide ELISAs .
1.7508 10.5401 1.0000 The data demonstrate a remarkable qualitative and quantitative heterogeneity of the humoral HBx immune response which can be monitored by proteinHBx -specific peptide ELISAs .
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Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5491 10.8781 0.9999 [The inhibitory effect of hydrocortisone on the chemotactic migration of cell_typehuman leukocytes ]
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1.6834 10.6493 1.0000 Random migration ( RM ) and chemotactic migration ( ChtM ) of cell_typehuman leukocytes to yeast activated serum were studied with the modified Boyden chamber method .
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0.9140 1.0000 1.0000 cell_typeLeukocytes migrated most rapidly at night.
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0.7127 1.0000 1.0000 The difference between the peak (0:00) and trough values (8:00) of RM and proteinChtM was significant statistically (P less than 0.01).
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0.9860 1.0000 1.0000 proteinChtM was inhibited by hydrocortisone (F) of physiological concentration (10(-9)-10(-7) mol/L) which was dose-dependent and completely antagonized by the competitive antagonist , RU38486 .
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0.9134 1.0000 1.0000 It is suggested that glucocorticoids ( GC ) may be a physiological regulator of the activity of cell_typeleukocytes and its inhibitory action on ChtM may be involved in antiinflammatory mechanisms of GC of pharmacological doses .
1.8221 10.3103 1.0000 It is suggested that glucocorticoids ( GC ) may be a physiological regulator of the activity of leukocytes and its inhibitory action on proteinChtM may be involved in antiinflammatory mechanisms of GC of pharmacological doses .
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3.0738 20.9108 20.9026 The action of physiological and pharmacological concentration of GC may be mediated by proteinlow affinity specific binding sites of glucocorticoid receptors .
1.4667 10.9204 0.9997 The action of physiological and pharmacological concentration of GC may be mediated by low affinity specific binding sites of proteinglucocorticoid receptors .
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3.4748 20.1175 10.5259 Heterogeneity of antigen molecules recognized by proteinanti-tax1 monoclonal antibody Lt-4 in cell lines bearing human T cell leukemia virus type I and related retroviruses .
1.4411 10.8021 1.0000 Heterogeneity of proteinantigen molecules recognized by anti-tax1 monoclonal antibody Lt-4 in cell lines bearing human T cell leukemia virus type I and related retroviruses .
2.0833 20.1971 0.9997 Heterogeneity of antigen molecules recognized by proteinanti-tax1 monoclonal antibody Lt-4 in cell lines bearing human T cell leukemia virus type I and related retroviruses .
1.6144 10.3568 1.0000 Heterogeneity of antigen molecules recognized by anti-tax1 monoclonal antibody Lt-4 in cell_linecell lines bearing human T cell leukemia virus type I and related retroviruses .
Heterogeneity of antigen molecules recognized by anti-tax1 monoclonal antibody proteinLt-4 in cell lines bearing human T cell leukemia virus type I and related retroviruses .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6140 10.7094 1.0000 Using a monoclonal antibody , Lt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of proteintax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
1.3508 20.6713 0.9999 Using a proteinmonoclonal antibody , Lt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
0.9825 1.0000 0.9790 Using a monoclonal antibody , Lt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( proteintax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
0.9169 0.9999 1.0000 Using a monoclonal antibody , proteinLt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
0.7384 0.9873 0.9963 Using a monoclonal antibody , Lt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of cell_lineT cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
Using a monoclonal antibody , Lt-4 , directed against proteinhuman T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
Using a monoclonal antibody , Lt-4 , directed against proteinhuman T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
Using a monoclonal antibody , Lt-4 , directed against human T cell leukemia virus type I ( HTLV-I ) trans-activator ( tax1 ) antigen , we examined the expression of tax1 and related proteinantigens in a variety of T cell lines bearing HTLV-I and related retroviruses , simian T cell leukemia virus type I ( STLV-I ) and HTLV-II , by immunofluorescence and immunoblot assays .
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4.0490 20.9964 10.8062 Lt-4 reacted with all HTLV-I -bearing cell lines tested and five out of eight simian cell lines bearing STLV-I , but not with an cell_lineHTLV-II -bearing cell line .
3.8978 20.5606 10.8953 Lt-4 reacted with all cell_lineHTLV-I -bearing cell lines tested and five out of eight simian cell lines bearing STLV-I , but not with an HTLV-II -bearing cell line .
3.6956 20.5421 10.7379 Lt-4 reacted with all HTLV-I -bearing cell lines tested and five out of eight cell_linesimian cell lines bearing STLV-I , but not with an HTLV-II -bearing cell line .
0.9638 1.0000 1.0000 proteinLt-4 reacted with all HTLV-I -bearing cell lines tested and five out of eight simian cell lines bearing STLV-I , but not with an HTLV-II -bearing cell line .
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4.8786 30.9207 10.7214 Lt-4 detected 40 kd tax1 antigen molecules in most cell_lineHTLV-I -bearing cell lines except one cell line that expressed 39 kd tax1 antigen .
3.9890 30.5884 10.4108 Lt-4 detected 40 kd tax1 antigen molecules in most HTLV-I -bearing cell lines except one cell line that expressed protein39 kd tax1 antigen .
0.9336 1.0000 1.0000 proteinLt-4 detected 40 kd tax1 antigen molecules in most HTLV-I -bearing cell lines except one cell line that expressed 39 kd tax1 antigen .
3.8664 20.1534 20.2734 Lt-4 detected protein40 kd tax1 antigen molecules in most HTLV-I -bearing cell lines except one cell line that expressed 39 kd tax1 antigen .
Lt-4 detected 40 kd proteintax1 antigen molecules in most HTLV-I -bearing cell lines except one cell line that expressed 39 kd tax1 antigen .
Lt-4 detected 40 kd proteintax1 antigen molecules in most HTLV-I -bearing cell lines except one cell line that expressed 39 kd tax1 antigen .
Lt-4 detected 40 kd tax1 antigen molecules in most HTLV-I -bearing cell lines except one cell line that expressed 39 kd proteintax1 antigen .
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5.5950 20.5086 20.9913 In the cell_lineSTLV-I -bearing T cell lines , tax1 -related antigen molecules detected by Lt-4 were heterogeneous, having molecular weights in the range of 36-41 kd.
4.0112 20.8286 10.6848 In the STLV-I -bearing T cell lines , proteintax1 -related antigen molecules detected by Lt-4 were heterogeneous, having molecular weights in the range of 36-41 kd.
1.6669 10.1201 0.9956 In the STLV-I -bearing T cell lines , proteintax1 -related antigen molecules detected by Lt-4 were heterogeneous, having molecular weights in the range of 36-41 kd.
0.8411 1.0000 1.0000 In the STLV-I -bearing T cell lines , tax1 -related antigen molecules detected by proteinLt-4 were heterogeneous, having molecular weights in the range of 36-41 kd.
In the STLV-I -bearing cell_lineT cell lines , tax1 -related antigen molecules detected by Lt-4 were heterogeneous, having molecular weights in the range of 36-41 kd.
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7.3853 30.0178 30.2250 Characterization of the proteinhuman immunodeficiency virus type 1 enhancer -binding proteins from the human T-cell line Jurkat .
4.2014 30.5784 10.7919 Characterization of the human immunodeficiency virus type 1 enhancer -binding proteins from the cell_linehuman T-cell line Jurkat .
Characterization of the DNAhuman immunodeficiency virus type 1 enhancer -binding proteins from the human T-cell line Jurkat .
Characterization of the human immunodeficiency virus type 1 enhancer -binding proteins from the cell_linehuman T-cell line Jurkat .
Characterization of the human immunodeficiency virus type 1 enhancer -binding proteins from the human T-cell line cell_lineJurkat .
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3.2769 20.8138 10.7681 The transcription of the human immunodeficiency virus type 1 ( HIV-1 ) is under the control of cellular proteins that bind to the DNAviral long terminal repeat ( LTR ).
1.5418 10.9295 1.0000 The transcription of the human immunodeficiency virus type 1 ( HIV-1 ) is under the control of proteincellular proteins that bind to the viral long terminal repeat ( LTR ).
0.9364 1.0000 1.0000 The transcription of the human immunodeficiency virus type 1 ( HIV-1 ) is under the control of cellular proteins that bind to the viral long terminal repeat ( DNALTR ).
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1.3971 10.9792 0.9998 Among the protein-binding regions of the HIV-1 LTR is the DNAtranscription-enhancer region .
1.3618 10.9171 0.9999 Among the protein-binding regions of the DNAHIV-1 LTR is the transcription-enhancer region .
1.3526 10.7480 0.9999 Among the proteinprotein-binding regions of the HIV-1 LTR is the transcription-enhancer region .
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2.2197 20.2579 0.9999 We show that at least one inducible , C1 , and one constitutive, C2 , protein can bind to the DNAHIV enhancer in Jurkat cells .
1.6860 10.5149 1.0000 We show that at least one inducible , proteinC1 , and one constitutive, C2 , protein can bind to the HIV enhancer in Jurkat cells .
1.6170 10.8190 0.9998 We show that at least one inducible , C1 , and one constitutive, C2 , protein can bind to the HIV enhancer in cell_lineJurkat cells .
0.9134 1.0000 1.0000 We show that at least one inducible , C1 , and one constitutive, proteinC2 , protein can bind to the HIV enhancer in Jurkat cells .
We show that at least one proteininducible , C1 , and one constitutive, C2 , protein can bind to the HIV enhancer in Jurkat cells .
We show that at least one inducible , C1 , and one proteinconstitutive, C2 , protein can bind to the HIV enhancer in Jurkat cells .
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2.4041 20.4713 0.9999 Bivalent cations such as Mg2+ and Zn2+ differentially affect their binding to oligonucleotides which contain the DNAHIV-enhancer domain .
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3.9651 20.9771 10.7526 Both C1 and C2 proteins also bind to a similar sequence found in the DNAinterleukin-2 -receptor alpha-subunit enhancer .
2.1543 20.2212 0.9972 Both C1 and C2 proteins also bind to a similar sequence found in the proteininterleukin-2 -receptor alpha-subunit enhancer .
0.8765 1.0000 1.0000 Both proteinC1 and C2 proteins also bind to a similar sequence found in the interleukin-2 -receptor alpha-subunit enhancer .
0.7514 0.9960 0.9999 Both C1 and proteinC2 proteins also bind to a similar sequence found in the interleukin-2 -receptor alpha-subunit enhancer .
Both C1 and C2 proteins also bind to a similar sequence found in the proteininterleukin-2 -receptor alpha-subunit enhancer .
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2.9501 20.9378 10.9760 The inducible C1 protein was partially purified by three chromatographic steps and characterized by u.v. cross-linking as a protein47 kDa protein .
2.2549 20.5532 1.0000 The inducible proteinC1 protein was partially purified by three chromatographic steps and characterized by u.v. cross-linking as a 47 kDa protein .
The proteininducible C1 protein was partially purified by three chromatographic steps and characterized by u.v. cross-linking as a 47 kDa protein .
The inducible proteinC1 protein was partially purified by three chromatographic steps and characterized by u.v. cross-linking as a 47 kDa protein .
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1.4405 10.9309 1.0000 Differences in DNAtranscriptional enhancers of HIV-1 and HIV-2 .
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Response to cell_typeT cell activation signals .
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cell_typeT cell activation results in high levels of HIV replication and is thought to be one mechanism leading to the conversion from latent to active viral infection .
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5.2415 30.0349 10.4828 In HIV-1 , the sequences that respond to these signaling events are found in the long terminal repeat ( LTR ) and comprise the transcriptional enhancer , which contains two conserved binding sites for the proteinnuclear factor kappa B ( NF kappa B ).
4.0455 20.8621 10.6820 In HIV-1 , the sequences that respond to these signaling events are found in the long terminal repeat ( LTR ) and comprise the transcriptional enhancer , which contains two DNAconserved binding sites for the nuclear factor kappa B ( NF kappa B ).
3.9441 20.7396 10.6344 In HIV-1 , the sequences that respond to these signaling events are found in the long terminal repeat ( LTR ) and comprise the transcriptional enhancer , which contains two conserved binding sites for the nuclear factor kappa B ( proteinNF kappa B ).
3.5211 20.7428 10.8391 In HIV-1 , the sequences that respond to these signaling events are found in the DNAlong terminal repeat ( LTR ) and comprise the transcriptional enhancer , which contains two conserved binding sites for the nuclear factor kappa B ( NF kappa B ).
2.0654 20.2623 1.0000 In HIV-1 , the sequences that respond to these signaling events are found in the long terminal repeat ( LTR ) and comprise the DNAtranscriptional enhancer , which contains two conserved binding sites for the nuclear factor kappa B ( NF kappa B ).
0.9524 1.0000 1.0000 In HIV-1 , the sequences that respond to these signaling events are found in the long terminal repeat ( DNALTR ) and comprise the transcriptional enhancer , which contains two conserved binding sites for the nuclear factor kappa B ( NF kappa B ).
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4.1127 20.7390 10.9582 The corresponding region in the second AIDS retrovirus , HIV-2 , contains a conserved and a divergent DNANF kappa B binding site .
3.2183 20.9643 10.9526 The corresponding region in the second AIDS retrovirus , HIV-2 , contains a conserved and a divergent proteinNF kappa B binding site .
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2.2947 20.2056 1.0000 We demonstrate that the HIV-1 LTR responds better than the DNAHIV-2 LTR to T cell activation signals.
2.2919 20.1200 0.9999 We demonstrate that the DNAHIV-1 LTR responds better than the HIV-2 LTR to T cell activation signals.
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1.7313 10.5361 1.0000 These qualitative differences in the response to T cell activation are reproduced not only when HIV-1 or HIV-2 enhancers are placed upstream of a DNAheterologous promoter but also when these enhancers are switched between their respective LTR .
0.8841 1.0000 1.0000 These qualitative differences in the response to T cell activation are reproduced not only when HIV-1 or HIV-2 enhancers are placed upstream of a heterologous promoter but also when these enhancers are switched between their respective DNALTR .
0.7377 1.0000 1.0000 These qualitative differences in the response to T cell activation are reproduced not only when HIV-1 or HIV-2 enhancers are placed upstream of a heterologous promoter but also when these DNAenhancers are switched between their respective LTR .
These qualitative differences in the response to cell_typeT cell activation are reproduced not only when HIV-1 or HIV-2 enhancers are placed upstream of a heterologous promoter but also when these enhancers are switched between their respective LTR .
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3.6048 20.8111 10.7573 In electrophoretic mobility shift assays, NF kappa B binds to both conserved sites in the DNAHIV-1 transcriptional enhancer and only to the single conserved site in the HIV-2 transcriptional enhancer .
3.5730 20.7379 10.9688 In electrophoretic mobility shift assays, NF kappa B binds to both conserved sites in the HIV-1 transcriptional enhancer and only to the single conserved site in the DNAHIV-2 transcriptional enhancer .
2.1118 20.5732 10.0399 In electrophoretic mobility shift assays, proteinNF kappa B binds to both conserved sites in the HIV-1 transcriptional enhancer and only to the single conserved site in the HIV-2 transcriptional enhancer .
2.0601 20.0780 0.9999 In electrophoretic mobility shift assays, NF kappa B binds to both conserved sites in the HIV-1 transcriptional enhancer and only to the single DNAconserved site in the HIV-2 transcriptional enhancer .
1.3851 10.9676 0.9998 In electrophoretic mobility shift assays, NF kappa B binds to both DNAconserved sites in the HIV-1 transcriptional enhancer and only to the single conserved site in the HIV-2 transcriptional enhancer .
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4.0040 20.2649 10.5744 Instead of proteinNF kappa B , the activator protein 3 binds to the divergent site in HIV-2 .
3.4000 20.2320 10.7174 Instead of NF kappa B , the proteinactivator protein 3 binds to the divergent site in HIV-2 .
2.0105 20.4829 0.9999 Instead of NF kappa B , the activator protein 3 binds to the DNAdivergent site in HIV-2 .
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2.7149 10.6290 10.5181 NF-X2 that binds to the DRA X2-box is proteinactivator protein 1 .
1.2543 10.7677 0.9996 NF-X2 that binds to the DNADRA X2-box is activator protein 1 .
0.9068 1.0000 1.0000 proteinNF-X2 that binds to the DRA X2-box is activator protein 1 .
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1.2371 10.3260 1.0000 Expression cloning of proteinc-Jun .
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2.8802 20.8695 10.5375 Human class II MHC Ag are a family of proteincell surface glycoproteins .
2.4073 0.9992 20.6562 proteinHuman class II MHC Ag are a family of cell surface glycoproteins .
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2.7344 10.8696 10.9884 Their constitutive expression is limited to B lymphocytes and cell_typethymic epithelial cells .
1.2774 10.8579 0.9994 Their constitutive expression is limited to cell_typeB lymphocytes and thymic epithelial cells .
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1.5690 10.9267 1.0000 In many other cells their expression can be induced by proteinIFN-gamma .
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3.3241 20.7678 10.4933 Conserved upstream promoter sequences regulate this tissue-specific expression of DNAclass II genes .
2.6905 10.8237 10.5207 Conserved DNAupstream promoter sequences regulate this tissue-specific expression of class II genes .
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4.2267 20.9413 10.8058 In the DRA promoter , one of these cis-acting regulatory motifs is the X2-box to which proteinnuclear factor X2 ( NF-X2 ) binds.
3.9437 20.8168 10.8492 In the DRA promoter , one of these DNAcis-acting regulatory motifs is the X2-box to which nuclear factor X2 ( NF-X2 ) binds.
2.1332 20.1449 1.0000 In the DRA promoter , one of these cis-acting regulatory motifs is the DNAX2-box to which nuclear factor X2 ( NF-X2 ) binds.
1.3303 20.9372 0.9999 In the DNADRA promoter , one of these cis-acting regulatory motifs is the X2-box to which nuclear factor X2 ( NF-X2 ) binds.
0.9590 1.0000 0.9999 In the DRA promoter , one of these cis-acting regulatory motifs is the X2-box to which nuclear factor X2 ( proteinNF-X2 ) binds.
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3.7216 20.5438 10.5418 Here, we present the isolation and characterization of the DNAfull-length cDNA clone encoding NF-X2 .
0.8729 0.9999 1.0000 Here, we present the isolation and characterization of the full-length cDNA clone encoding proteinNF-X2 .
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5.3299 30.1432 10.7262 This cDNA clone was isolated by expression cDNA cloning , and encodes the human c-Jun protein , which together with c-Fos forms the proteinheterodimeric activator protein-1 transcription complex .
2.1995 20.5719 0.9999 This cDNA clone was isolated by expression cDNA cloning , and encodes the proteinhuman c-Jun protein , which together with c-Fos forms the heterodimeric activator protein-1 transcription complex .
1.3788 10.8373 0.9999 This DNAcDNA clone was isolated by expression cDNA cloning , and encodes the human c-Jun protein , which together with c-Fos forms the heterodimeric activator protein-1 transcription complex .
1.3658 10.0393 1.0000 This cDNA clone was isolated by expression cDNA cloning , and encodes the human c-Jun protein , which together with proteinc-Fos forms the heterodimeric activator protein-1 transcription complex .
0.8569 1.0000 0.9871 This cDNA clone was isolated by expression cDNA cloning , and encodes the human proteinc-Jun protein , which together with c-Fos forms the heterodimeric activator protein-1 transcription complex .
This cDNA clone was isolated by expression DNAcDNA cloning , and encodes the human c-Jun protein , which together with c-Fos forms the heterodimeric activator protein-1 transcription complex .
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2.0928 10.5105 10.7668 Whereas proteinc-Fos /c-Jun heterodimers do not exist in B cells , they form and bind to the X2-box in class II nonexpressing cells .
1.4069 10.8301 0.9999 Whereas c-Fos /c-Jun heterodimers do not exist in B cells , they form and bind to the DNAX2-box in class II nonexpressing cells .
0.6797 0.9999 0.9937 Whereas proteinc-Fos /c-Jun heterodimers do not exist in B cells , they form and bind to the X2-box in class II nonexpressing cells .
4.5286 20.4637 10.2439 Whereas c-Fos /c-Jun heterodimers do not exist in B cells , they form and bind to the X2-box in cell_typeclass II nonexpressing cells .
1.9541 20.8028 0.9998 Whereas c-Fos /c-Jun heterodimers do not exist in cell_typeB cells , they form and bind to the X2-box in class II nonexpressing cells .
Whereas c-Fos /c-Jun heterodimers do not exist in cell_lineB cells , they form and bind to the X2-box in class II nonexpressing cells .
Whereas c-Fos /c-Jun heterodimers do not exist in B cells , they form and bind to the X2-box in cell_lineclass II nonexpressing cells .
Whereas c-Fos protein/c-Jun heterodimers do not exist in B cells , they form and bind to the X2-box in class II nonexpressing cells .
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2.1150 10.8077 10.1779 Thus, proteinc-Fos /c-Jun heterodimers might contribute to the repression of DRA gene expression .
2.0119 20.6797 0.9999 Thus, c-Fos /c-Jun heterodimers might contribute to the repression of DNADRA gene expression .
0.6747 0.9999 0.9953 Thus, proteinc-Fos /c-Jun heterodimers might contribute to the repression of DRA gene expression .
Thus, c-Fos protein/c-Jun heterodimers might contribute to the repression of DRA gene expression .
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2.8706 10.9804 10.5831 Radioreceptor assay of some corticosteroid derivatives in cell_typehuman mononuclear leukocytes .
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3.5843 20.4239 10.7105 Several new 4,19-substituted steroids and previously synthesized corticosteroids were assayed for affinity to proteintype 1 receptors in human mononuclear leukocytes .
2.9757 10.9551 10.4905 Several new 4,19-substituted steroids and previously synthesized corticosteroids were assayed for affinity to type 1 receptors in cell_typehuman mononuclear leukocytes .
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3.9386 20.8004 10.3941 When tested in a radioreceptor assay in human mononuclear leukocytes the synthesized compounds showed only low relative binding affinities ( RBA ) to proteintype 1 receptor , the highest being 0.72% for 13 ( aldosterone = 100%).
3.0652 30.0654 10.7278 When tested in a radioreceptor assay in cell_typehuman mononuclear leukocytes the synthesized compounds showed only low relative binding affinities ( RBA ) to type 1 receptor , the highest being 0.72% for 13 ( aldosterone = 100%).
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0.9332 1.0000 1.0000 For comparison, other proteinRBA in this system were: 19-noraldosterone , 20%; 18-deoxyaldosterone , 5.8%; 18-deoxy-19-noraldosterone , 4.7%; 18,21-anhydroaldosterone , 0.37%; 17-isoaldosterone , 7.6% and apoaldosterone , 4.3%
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2.1377 20.9584 0.9998 Cell type specificity and activation requirements for NFAT-1 ( nuclear factor of activated T-cells ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual proteinnuclear factor .
1.4786 10.9753 1.0000 Cell type specificity and activation requirements for proteinNFAT-1 ( nuclear factor of activated T-cells ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual nuclear factor .
5.0420 30.4423 20.8982 Cell type specificity and activation requirements for NFAT-1 ( proteinnuclear factor of activated T-cells ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual nuclear factor .
Cell type specificity and activation requirements for NFAT-1 ( nuclear factor of cell_typeactivated T-cells ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual nuclear factor .
Cell type specificity and activation requirements for NFAT-1 ( proteinnuclear factor of activated T-cells ) transcriptional activity determined by a new method using transgenic mice to assay transcriptional activity of an individual nuclear factor .
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1.9390 20.8680 1.0000 Nuclear factor of activated T-cells ( NFAT-1 ) is a proteintranscription factor which is considered to be an important regulator in early T-cell activation .
0.9791 1.0000 1.0000 Nuclear factor of activated T-cells ( proteinNFAT-1 ) is a transcription factor which is considered to be an important regulator in early T-cell activation .
2.4029 0.9995 20.5539 proteinNuclear factor of activated T-cells ( NFAT-1 ) is a transcription factor which is considered to be an important regulator in early T-cell activation .
proteinNuclear factor of activated T-cells ( NFAT-1 ) is a transcription factor which is considered to be an important regulator in early T-cell activation .
Nuclear factor of cell_typeactivated T-cells ( NFAT-1 ) is a transcription factor which is considered to be an important regulator in early T-cell activation .
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2.5234 20.1680 1.0000 We have developed a system to monitor the transcriptional activity of proteinNFAT-1 at the single cell level in whole animals .
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0.9134 1.0000 0.9964 The system is based on the use of an oligomerized proteinNFAT-1 binding motif that directs transcription of SV40 T-antigen in transgenic mice .
3.9887 20.8308 10.7168 The system is based on the use of an DNAoligomerized NFAT-1 binding motif that directs transcription of SV40 T-antigen in transgenic mice .
1.7836 20.7408 1.0000 The system is based on the use of an oligomerized NFAT-1 binding motif that directs transcription of proteinSV40 T-antigen in transgenic mice .
The system is based on the use of an oligomerized NFAT-1 binding motif that directs proteintranscription of SV40 T-antigen in transgenic mice .
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2.5601 20.7522 10.8654 This report represents the first demonstration that a proteinmultimerized short binding motif can function appropriately in transgenic mice .
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2.8408 20.8207 10.1225 NFAT-1 activity had previously been thought to be confined to cell_typeactivated T-lymphocytes upon release of intracellular calcium .
0.9615 1.0000 1.0000 proteinNFAT-1 activity had previously been thought to be confined to activated T-lymphocytes upon release of intracellular calcium .
NFAT-1 activity had previously been thought to be confined to activated T-lymphocytes upon release of cell_typeintracellular calcium .
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1.7209 10.8370 1.0000 By targeting proteinNFAT-1 -dependent gene expression in transgenic mice we discovered new sites of NFAT-1 activity .
1.6331 10.8190 1.0000 By targeting NFAT-1 -dependent gene expression in transgenic mice we discovered new sites of proteinNFAT-1 activity .
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3.4731 20.9864 10.8496 Besides in T-lymphocytes NFAT-1 activity could also be induced in T-lymphocyte-depleted spleen cells and purified B-lymphocytes and requires agents that both release intracellular calcium and activate proteinprotein kinase C .
1.4459 10.9593 0.9996 Besides in cell_typeT-lymphocytes NFAT-1 activity could also be induced in T-lymphocyte-depleted spleen cells and purified B-lymphocytes and requires agents that both release intracellular calcium and activate protein kinase C .
0.9202 1.0000 1.0000 Besides in T-lymphocytes proteinNFAT-1 activity could also be induced in T-lymphocyte-depleted spleen cells and purified B-lymphocytes and requires agents that both release intracellular calcium and activate protein kinase C .
3.2884 20.5266 10.6901 Besides in T-lymphocytes NFAT-1 activity could also be induced in cell_lineT-lymphocyte-depleted spleen cells and purified B-lymphocytes and requires agents that both release intracellular calcium and activate protein kinase C .
1.1256 10.5856 0.9992 Besides in T-lymphocytes NFAT-1 activity could also be induced in T-lymphocyte-depleted spleen cells and cell_linepurified B-lymphocytes and requires agents that both release intracellular calcium and activate protein kinase C .
Besides in T-lymphocytes NFAT-1 activity could also be induced in cell_typeT-lymphocyte-depleted spleen cells and purified B-lymphocytes and requires agents that both release intracellular calcium and activate protein kinase C .
Besides in T-lymphocytes NFAT-1 activity could also be induced in T-lymphocyte-depleted spleen cells and cell_typepurified B-lymphocytes and requires agents that both release intracellular calcium and activate protein kinase C .
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1.5672 10.5842 1.0000 A difference in the time course of appearance of NFAT-1 activity between cell_typeT-lymphocytes and non-T-lymphocytes was revealed.
1.5442 10.7960 1.0000 A difference in the time course of appearance of proteinNFAT-1 activity between T-lymphocytes and non-T-lymphocytes was revealed.
0.8656 0.9999 1.0000 A difference in the time course of appearance of NFAT-1 activity between T-lymphocytes and cell_typenon-T-lymphocytes was revealed.
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1.7930 10.7037 1.0000 Interestingly, the tissue pattern of expression of the proteinNFAT-1 activity resembles the expression pattern described for HIV-LTR/tat transgenic mice (Vogel, J., Hinrichs, S. H., Reynolds, R. K., Luciw, P. A., and Jay, G. (1988) Nature 335, 606-611).
1.2709 10.1710 1.0000 Interestingly, the tissue pattern of expression of the NFAT-1 activity resembles the expression pattern described for DNAHIV-LTR/tat transgenic mice (Vogel, J., Hinrichs, S. H., Reynolds, R. K., Luciw, P. A., and Jay, G. (1988) Nature 335, 606-611).
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1.6553 10.3691 1.0000 This similarity in expression and the fact that NFAT-1 has been shown to bind functional sequences in HIV-LTR suggest a role for proteinNFAT-1 in dermal activation of the HIV-LTR .
1.6548 10.5540 1.0000 This similarity in expression and the fact that proteinNFAT-1 has been shown to bind functional sequences in HIV-LTR suggest a role for NFAT-1 in dermal activation of the HIV-LTR .
1.5664 10.6499 1.0000 This similarity in expression and the fact that NFAT-1 has been shown to bind functional sequences in HIV-LTR suggest a role for NFAT-1 in dermal activation of the DNAHIV-LTR .
1.5485 10.8614 0.9999 This similarity in expression and the fact that NFAT-1 has been shown to bind DNAfunctional sequences in HIV-LTR suggest a role for NFAT-1 in dermal activation of the HIV-LTR .
0.8889 1.0000 1.0000 This similarity in expression and the fact that NFAT-1 has been shown to bind functional sequences in DNAHIV-LTR suggest a role for NFAT-1 in dermal activation of the HIV-LTR .
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6.1751 30.6166 20.6394 A novel T-cell protein which recognizes a palindromic sequence in the negative regulatory element of the DNAhuman immunodeficiency virus long terminal repeat .
3.5920 20.7198 10.8930 A novel T-cell protein which recognizes a palindromic sequence in the DNAnegative regulatory element of the human immunodeficiency virus long terminal repeat .
1.7538 20.3963 0.9999 A novel T-cell protein which recognizes a DNApalindromic sequence in the negative regulatory element of the human immunodeficiency virus long terminal repeat .
1.3138 10.5815 0.9991 A proteinnovel T-cell protein which recognizes a palindromic sequence in the negative regulatory element of the human immunodeficiency virus long terminal repeat .
A novel proteinT-cell protein which recognizes a palindromic sequence in the negative regulatory element of the human immunodeficiency virus long terminal repeat .
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7.2969 30.9175 20.6221 Two major protein-binding sites within the negative regulatory element of the DNAhuman immunodeficiency virus type 1 long terminal repeat have been identified.
2.9722 20.2840 10.6575 Two major protein-binding sites within the DNAnegative regulatory element of the human immunodeficiency virus type 1 long terminal repeat have been identified.
1.7424 20.5653 0.9999 Two major DNAprotein-binding sites within the negative regulatory element of the human immunodeficiency virus type 1 long terminal repeat have been identified.
Two DNAmajor protein-binding sites within the negative regulatory element of the human immunodeficiency virus type 1 long terminal repeat have been identified.
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3.8750 20.6766 10.9061 One ( site B ) contained a palindromic sequence with homology to DNAsteroid/thyroid hormone response elements but was distinct from previously described binding sites of this class.
1.4236 10.9039 0.9999 One ( DNAsite B ) contained a palindromic sequence with homology to steroid/thyroid hormone response elements but was distinct from previously described binding sites of this class.
1.2988 10.9772 1.0000 One ( site B ) contained a DNApalindromic sequence with homology to steroid/thyroid hormone response elements but was distinct from previously described binding sites of this class.
1.4020 10.7781 0.9999 One ( site B ) contained a palindromic sequence with homology to steroid/thyroid hormone response elements but was distinct from previously described DNAbinding sites of this class.
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1.6261 10.5430 1.0000 A novel proteinT-cell protein recognized the palindromic sequence within site B and also bound estrogen- or thyroid hormone- response elements with lower affinity.
1.5674 10.7152 0.9999 A novel T-cell protein recognized the palindromic sequence within DNAsite B and also bound estrogen- or thyroid hormone- response elements with lower affinity.
1.4546 10.9558 0.9999 A novel T-cell protein recognized the DNApalindromic sequence within site B and also bound estrogen- or thyroid hormone- response elements with lower affinity.
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6.4727 30.7320 20.1418 A 7-base-pair mutation in the site B palindrome , which destroyed protein binding, resulted in increased expression from the DNAhuman immunodeficiency virus type 1 long terminal repeat in T cells .
4.1009 30.5306 10.7953 A 7-base-pair mutation in the DNAsite B palindrome , which destroyed protein binding, resulted in increased expression from the human immunodeficiency virus type 1 long terminal repeat in T cells .
1.4258 10.8413 0.9990 A 7-base-pair mutation in the site B palindrome , which destroyed protein binding, resulted in increased expression from the human immunodeficiency virus type 1 long terminal repeat in cell_typeT cells .
A 7-base-pair mutation in the DNAsite B palindrome , which destroyed protein binding, resulted in increased expression from the human immunodeficiency virus type 1 long terminal repeat in T cells .
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2.2401 20.2225 1.0000 Progesterone suppression of cell_typepregnancy lymphocytes is not mediated by glucocorticoid effect.
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2.3164 20.1538 1.0000 This study investigated whether the suppressive effect of progesterone on cell_typepregnancy lymphocytes is mediated by specific progesterone receptors .
2.2547 20.3675 0.9999 This study investigated whether the suppressive effect of progesterone on pregnancy lymphocytes is mediated by specific proteinprogesterone receptors .
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2.2690 20.5893 0.9998 The effects of a competitive progesterone antagonist ( RU486 ) and a specific proteinglucocorticoid receptor blocker ( RU43044 ) were tested on the release of a blocking factor by progesterone -treated pregnancy lymphocytes .
2.1235 20.2971 0.9999 The effects of a competitive progesterone antagonist ( RU486 ) and a specific glucocorticoid receptor blocker ( RU43044 ) were tested on the release of a proteinblocking factor by progesterone -treated pregnancy lymphocytes .
1.6906 0.9998 10.4090 The effects of a competitive progesterone antagonist ( RU486 ) and a specific glucocorticoid receptor blocker ( RU43044 ) were tested on the release of a blocking factor by progesterone -treated cell_typepregnancy lymphocytes .
2.2146 20.3895 10.3164 The effects of a competitive progesterone antagonist ( RU486 ) and a specific glucocorticoid receptor blocker ( RU43044 ) were tested on the release of a blocking factor by cell_typeprogesterone -treated pregnancy lymphocytes .
The effects of a competitive progesterone antagonist ( RU486 ) and a specific glucocorticoid receptor blocker ( RU43044 ) were tested on the release of a blocking factor by cell_lineprogesterone -treated pregnancy lymphocytes .
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2.5060 20.4505 1.0000 RU 486 tested at an equal concentration as progesterone significantly inhibited the production of the proteinblocking factor , while RU 43044 was without effect.
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3.0037 10.6974 10.4652 These data suggest that in pregnancy, lymphocyte progesterone acts on specific progesterone receptors and proteinglucocorticoid binding sites are not involved.
2.1686 20.0153 0.9999 These data suggest that in pregnancy, lymphocyte progesterone acts on specific proteinprogesterone receptors and glucocorticoid binding sites are not involved.
0.7306 0.9997 0.9999 These data suggest that in pregnancy, cell_typelymphocyte progesterone acts on specific progesterone receptors and glucocorticoid binding sites are not involved.
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1.6256 10.9003 1.0000 The protein56-59-kilodalton protein identified in untransformed steroid receptor complexes is a unique protein that exists in cytosol in a complex with both the 70- and 90- kilodalton heat shock proteins .
3.9291 20.3283 10.9834 The 56-59-kilodalton protein identified in untransformed proteinsteroid receptor complexes is a unique protein that exists in cytosol in a complex with both the 70- and 90- kilodalton heat shock proteins .
The 56-59-kilodalton protein identified in untransformed steroid receptor complexes is a proteinunique protein that exists in cytosol in a complex with both the 70- and 90- kilodalton heat shock proteins .
The 56-59-kilodalton protein identified in proteinuntransformed steroid receptor complexes is a unique protein that exists in cytosol in a complex with both the 70- and 90- kilodalton heat shock proteins .
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2.4094 20.2588 1.0000 It has previously been shown that 9S , untransformed progestin , estrogen , androgen , and glucocorticoid receptor complexes in rabbit uterine and liver cytosols contain a protein59-kDa protein [Tai, P.K., Maeda, Y., Nakao, K., Wakim, N.G., Duhring, J.L., & Faber, L.E.(1986) Biochemistry 25, 5269-5275].
0.9428 1.0000 1.0000 It has previously been shown that protein9S , untransformed progestin , estrogen , androgen , and glucocorticoid receptor complexes in rabbit uterine and liver cytosols contain a 59-kDa protein [Tai, P.K., Maeda, Y., Nakao, K., Wakim, N.G., Duhring, J.L., & Faber, L.E.(1986) Biochemistry 25, 5269-5275].
4.7713 30.0227 10.6476 It has previously been shown that 9S , untransformed progestin , estrogen , androgen , and proteinglucocorticoid receptor complexes in rabbit uterine and liver cytosols contain a 59-kDa protein [Tai, P.K., Maeda, Y., Nakao, K., Wakim, N.G., Duhring, J.L., & Faber, L.E.(1986) Biochemistry 25, 5269-5275].
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4.2359 20.9379 10.8210 In this work we show that the proteinmonoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with 9S , untransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
4.1342 20.9728 10.8933 In this work we show that the monoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with 9S , untransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with protein4S salt-transformed receptors .
3.4959 20.6212 10.8343 In this work we show that the monoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with 9S , untransformed glucocorticoid receptor complexes in cytosol prepared from cell_linehuman IM-9 lymphocytes but not with 4S salt-transformed receptors .
3.4088 20.2526 10.7838 In this work we show that the monoclonal antibody KN 382/EC1 raised against the proteinrabbit 59-kDa protein reacts with 9S , untransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
5.9342 30.5268 20.6879 In this work we show that the monoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with protein9S , untransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
1.5330 0.9995 10.0808 In this work we show that the monoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with 9S , untransformed proteinglucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
0.7805 0.9994 0.9999 In this work we show that the monoclonal antibody proteinKN 382/EC1 raised against the rabbit 59-kDa protein reacts with 9S , untransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
In this work we show that the monoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with protein9S , untransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
In this work we show that the monoclonal antibody KN 382/EC1 raised against the rabbit 59-kDa protein reacts with 9S , proteinuntransformed glucocorticoid receptor complexes in cytosol prepared from human IM-9 lymphocytes but not with 4S salt-transformed receptors .
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2.2247 20.6121 1.0000 The human protein recognized by the EC1 antibody is a protein56-kDa protein ( p56 ) of moderate abundance located predominantly in the cytoplasm by indirect immunofluorescence .
1.4082 20.8719 1.0000 The human protein recognized by the proteinEC1 antibody is a 56-kDa protein ( p56 ) of moderate abundance located predominantly in the cytoplasm by indirect immunofluorescence .
0.9749 1.0000 1.0000 The human protein recognized by the EC1 antibody is a 56-kDa protein ( proteinp56 ) of moderate abundance located predominantly in the cytoplasm by indirect immunofluorescence .
1.3898 10.1159 0.9999 The proteinhuman protein recognized by the EC1 antibody is a 56-kDa protein ( p56 ) of moderate abundance located predominantly in the cytoplasm by indirect immunofluorescence .
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1.6753 10.9522 1.0000 There are at least six isomorphs of proteinp56 by two-dimensional gel analysis .
There are at least six proteinisomorphs of p56 by two-dimensional gel analysis .
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3.5639 20.7947 10.9858 N-Terminal sequencing ( 20 amino acids ) shows that p56 is a proteinunique human protein .
1.5262 10.8994 1.0000 N-Terminal sequencing ( 20 amino acids ) shows that proteinp56 is a unique human protein .
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2.1299 20.0392 0.9985 When p56 is immunoadsorbed from cell_lineIM-9 cell cytosol , both the 70- and 90- kDa heat shock proteins are coadsorbed in an immune-specific manner .
0.9306 0.9999 1.0000 When proteinp56 is immunoadsorbed from IM-9 cell cytosol , both the 70- and 90- kDa heat shock proteins are coadsorbed in an immune-specific manner .
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2.0941 10.8635 10.4087 Neither proteinheat shock protein reacts directly with the EC1 antibody .
2.0117 20.4533 0.9999 Neither heat shock protein reacts directly with the proteinEC1 antibody .
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2.5761 20.0431 1.0000 We conclude that proteinp56 exists in cytosol in a higher order complex containing hsp70 and hsp90 , both of which in turn have been found to be associated with untransformed steroid receptors .
1.8014 10.2439 1.0000 We conclude that p56 exists in cytosol in a higher order complex containing proteinhsp70 and hsp90 , both of which in turn have been found to be associated with untransformed steroid receptors .
0.9699 1.0000 1.0000 We conclude that p56 exists in cytosol in a higher order complex containing hsp70 and proteinhsp90 , both of which in turn have been found to be associated with untransformed steroid receptors .
2.3167 20.6125 0.9999 We conclude that p56 exists in cytosol in a higher order complex containing hsp70 and hsp90 , both of which in turn have been found to be associated with untransformed proteinsteroid receptors .
We conclude that p56 exists in cytosol in a higher order complex containing hsp70 and hsp90 , both of which in turn have been found to be associated with proteinuntransformed steroid receptors .
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4.0756 20.6737 10.9446 Sequence-specific DNA binding of the proto-oncoprotein ets-1 defines a DNAtranscriptional activator sequence within the long terminal repeat of the Moloney murine sarcoma virus .
3.5077 20.5840 10.6554 Sequence-specific DNA binding of the proto-oncoprotein ets-1 defines a transcriptional activator sequence within the DNAlong terminal repeat of the Moloney murine sarcoma virus .
Sequence-specific DNA binding of the proto-oncoprotein proteinets-1 defines a transcriptional activator sequence within the long terminal repeat of the Moloney murine sarcoma virus .
Sequence-specific DNA binding of the proteinproto-oncoprotein ets-1 defines a transcriptional activator sequence within the long terminal repeat of the Moloney murine sarcoma virus .
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2.9203 10.8364 10.8099 The DNAets proto-oncogene family is a group of sequence-related genes whose normal cellular function is unknown.
2.1341 20.2079 1.0000 The ets proto-oncogene family is a group of DNAsequence-related genes whose normal cellular function is unknown.
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3.7054 20.1622 10.7242 In a study of cellular proteins involved in the transcriptional regulation of murine retroviruses in T lymphocytes , we have discovered that a member of the ets gene family encodes a proteinsequence-specific DNA-binding protein .
3.6054 20.4963 10.7217 In a study of cellular proteins involved in the transcriptional regulation of murine retroviruses in T lymphocytes , we have discovered that a member of the DNAets gene family encodes a sequence-specific DNA-binding protein .
1.4892 10.9869 0.9999 In a study of cellular proteins involved in the transcriptional regulation of murine retroviruses in cell_typeT lymphocytes , we have discovered that a member of the ets gene family encodes a sequence-specific DNA-binding protein .
1.4743 10.9015 1.0000 In a study of proteincellular proteins involved in the transcriptional regulation of murine retroviruses in T lymphocytes , we have discovered that a member of the ets gene family encodes a sequence-specific DNA-binding protein .
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6.5178 30.6721 20.2903 A mouse ets-1 cDNA clone was obtained by screening a DNAmouse thymus cDNA expression library with a double-stranded oligonucleotide probe representing 20 bp of the Moloney murine sarcoma virus ( MSV ) long terminal repeat ( LTR ).
1.4120 10.5313 0.9911 A DNAmouse ets-1 cDNA clone was obtained by screening a mouse thymus cDNA expression library with a double-stranded oligonucleotide probe representing 20 bp of the Moloney murine sarcoma virus ( MSV ) long terminal repeat ( LTR ).
0.9162 0.9998 0.9999 A mouse ets-1 cDNA clone was obtained by screening a mouse thymus cDNA expression library with a double-stranded oligonucleotide probe representing 20 bp of the Moloney murine sarcoma virus ( MSV ) long terminal repeat ( DNALTR ).
4.8513 20.8665 30.7236 A mouse ets-1 cDNA clone was obtained by screening a mouse thymus cDNA expression library with a double-stranded oligonucleotide probe representing 20 bp of the DNAMoloney murine sarcoma virus ( MSV ) long terminal repeat ( LTR ).
A mouse ets-1 cDNA clone was obtained by screening a mouse thymus cDNA expression library with a DNAdouble-stranded oligonucleotide probe representing 20 bp of the Moloney murine sarcoma virus ( MSV ) long terminal repeat ( LTR ).
A mouse ets-1 cDNA clone was obtained by screening a mouse thymus cDNA expression library with a double-stranded oligonucleotide probe representing 20 bp of the Moloney murine sarcoma virus ( MSV ) DNAlong terminal repeat ( LTR ).
A mouse proteinets-1 cDNA clone was obtained by screening a mouse thymus cDNA expression library with a double-stranded oligonucleotide probe representing 20 bp of the Moloney murine sarcoma virus ( MSV ) long terminal repeat ( LTR ).
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4.1608 20.5327 10.6425 The cDNA sequence has an 813-bp open reading frame ( ORF ) whose predicted amino acid sequence is 97.6% identical to the protein272 carboxy-terminal amino acids of the human ets-1 protein .
3.9788 30.3770 10.6886 The cDNA sequence has an 813-bp open reading frame ( ORF ) whose predicted amino acid sequence is 97.6% identical to the 272 carboxy-terminal amino acids of the proteinhuman ets-1 protein .
3.9670 20.3683 10.9492 The cDNA sequence has an 813-bp open reading frame ( ORF ) whose predicted proteinamino acid sequence is 97.6% identical to the 272 carboxy-terminal amino acids of the human ets-1 protein .
3.8706 20.6326 10.8244 The cDNA sequence has an DNA813-bp open reading frame ( ORF ) whose predicted amino acid sequence is 97.6% identical to the 272 carboxy-terminal amino acids of the human ets-1 protein .
1.3217 10.9057 0.9998 The DNAcDNA sequence has an 813-bp open reading frame ( ORF ) whose predicted amino acid sequence is 97.6% identical to the 272 carboxy-terminal amino acids of the human ets-1 protein .
0.9408 1.0000 1.0000 The cDNA sequence has an 813-bp open reading frame ( DNAORF ) whose predicted amino acid sequence is 97.6% identical to the 272 carboxy-terminal amino acids of the human ets-1 protein .
The cDNA sequence has an 813-bp open reading frame ( ORF ) whose predicted amino acid sequence is 97.6% identical to the 272 carboxy-terminal amino acids of the human proteinets-1 protein .
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4.1041 20.8185 10.6667 The ORF was expressed in bacteria , and the protein30-kD protein product was shown to bind DNA in a sequence-specific manner by mobility-shift assays , Southwestern blot analysis , and methylation interference .
0.9307 0.9999 1.0000 The DNAORF was expressed in bacteria , and the 30-kD protein product was shown to bind DNA in a sequence-specific manner by mobility-shift assays , Southwestern blot analysis , and methylation interference .
0.7020 1.0000 1.0000 The ORF was expressed in bacteria , and the 30-kD protein product was shown to bind DNADNA in a sequence-specific manner by mobility-shift assays , Southwestern blot analysis , and methylation interference .
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3.7785 20.3220 10.6303 A mutant LTR containing four base pair substitutions in the DNAets-1 binding site was constructed and was shown to have reduced binding in vitro.
1.6350 10.6093 0.9999 A DNAmutant LTR containing four base pair substitutions in the ets-1 binding site was constructed and was shown to have reduced binding in vitro.
A mutant LTR containing four base pair substitutions in the proteinets-1 binding site was constructed and was shown to have reduced binding in vitro.
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3.7277 20.2342 10.8809 Transcriptional efficiency of the MSV LTR promoter containing this disrupted DNAets-1 binding site was compared to the activity of a wild-type promoter in mouse T lymphocytes in culture, and 15- to 20-fold reduction in expression of a reporter gene was observed.
3.6862 20.6537 10.7437 Transcriptional efficiency of the DNAMSV LTR promoter containing this disrupted ets-1 binding site was compared to the activity of a wild-type promoter in mouse T lymphocytes in culture, and 15- to 20-fold reduction in expression of a reporter gene was observed.
3.0657 10.7012 10.8551 Transcriptional efficiency of the MSV LTR promoter containing this disrupted ets-1 binding site was compared to the activity of a wild-type promoter in cell_typemouse T lymphocytes in culture, and 15- to 20-fold reduction in expression of a reporter gene was observed.
2.0425 20.6660 0.9997 Transcriptional efficiency of the MSV LTR promoter containing this disrupted ets-1 binding site was compared to the activity of a wild-type promoter in mouse T lymphocytes in culture, and 15- to 20-fold reduction in expression of a DNAreporter gene was observed.
1.4298 10.8680 0.9998 Transcriptional efficiency of the MSV LTR promoter containing this disrupted ets-1 binding site was compared to the activity of a DNAwild-type promoter in mouse T lymphocytes in culture, and 15- to 20-fold reduction in expression of a reporter gene was observed.
Transcriptional efficiency of the MSV LTR promoter containing this disrupted ets-1 binding site was compared to the activity of a wild-type promoter in mouse cell_typeT lymphocytes in culture, and 15- to 20-fold reduction in expression of a reporter gene was observed.
Transcriptional efficiency of the MSV LTR promoter containing this disrupted proteinets-1 binding site was compared to the activity of a wild-type promoter in mouse T lymphocytes in culture, and 15- to 20-fold reduction in expression of a reporter gene was observed.
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3.6878 20.8758 10.7572 We propose that ets-1 functions as a transcriptional activator of mammalian type-C retroviruses and speculate that ets-related genes constitute a new group of proteineukaryotic DNA-binding proteins .
2.2001 20.1780 1.0000 We propose that ets-1 functions as a transcriptional activator of mammalian type-C retroviruses and speculate that DNAets-related genes constitute a new group of eukaryotic DNA-binding proteins .
2.2885 20.0001 1.0000 We propose that DNAets-1 functions as a transcriptional activator of mammalian type-C retroviruses and speculate that ets-related genes constitute a new group of eukaryotic DNA-binding proteins .
We propose that proteinets-1 functions as a transcriptional activator of mammalian type-C retroviruses and speculate that ets-related genes constitute a new group of eukaryotic DNA-binding proteins .
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3.9894 10.7548 20.4204 Type II estrogen binding sites in cell_typehuman peripheral blood mononuclear cells : variations during the menstrual cycle .
2.3190 0.9981 20.6010 proteinType II estrogen binding sites in human peripheral blood mononuclear cells : variations during the menstrual cycle .
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5.8909 30.2239 20.0915 We have previously reported that cell_typehuman peripheral blood mononuclear cells ( PBMC ) contain type II estrogen binding sites ( type II EBS ).
2.0591 10.6847 10.0973 We have previously reported that human peripheral blood mononuclear cells ( PBMC ) contain type II estrogen binding sites ( proteintype II EBS ).
0.8891 0.9999 0.9999 We have previously reported that human peripheral blood mononuclear cells ( cell_typePBMC ) contain type II estrogen binding sites ( type II EBS ).
3.6388 20.7256 10.8212 We have previously reported that human peripheral blood mononuclear cells ( PBMC ) contain proteintype II estrogen binding sites ( type II EBS ).
We have previously reported that human peripheral blood mononuclear cells ( PBMC ) contain type proteinII estrogen binding sites ( type II EBS ).
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3.1932 20.8483 10.4213 In this study, the fluctuations of proteintype II EBS during the menstrual cycle were analyzed in 6 normally menstruating women .
0.6246 1.0000 1.0000 In this study, the fluctuations of type II proteinEBS during the menstrual cycle were analyzed in 6 normally menstruating women .
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3.1033 20.9672 10.8137 Approximately 3 times higher levels of proteintype II EBS were found in the periovulatory period with respect to both follicular and luteal phases .
0.9282 1.0000 1.0000 Approximately 3 times higher levels of type II proteinEBS were found in the periovulatory period with respect to both follicular and luteal phases .
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3.8049 20.7906 10.7255 In postmenopausal women the mean proteintype II EBS levels were similar to those observed in the follicular phase of the cycle.
0.7391 1.0000 1.0000 In postmenopausal women the mean type II proteinEBS levels were similar to those observed in the follicular phase of the cycle.
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2.6449 20.6631 10.8862 However, in 3 postmenopausal patients a short course of estrogen or tamoxifen resulted in a marked increase of proteintype II EBS levels.
0.9737 1.0000 1.0000 However, in 3 postmenopausal patients a short course of estrogen or tamoxifen resulted in a marked increase of type II proteinEBS levels.
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2.0512 20.4523 10.8977 Tamoxifen was also found to compete with 17 beta-estradiol for proteintype II EBS in PBMC , although to a lesser extent than diethylstilbestrol .
0.9456 0.9999 1.0000 Tamoxifen was also found to compete with 17 beta-estradiol for type II EBS in cell_typePBMC , although to a lesser extent than diethylstilbestrol .
0.9581 1.0000 1.0000 Tamoxifen was also found to compete with 17 beta-estradiol for type II proteinEBS in PBMC , although to a lesser extent than diethylstilbestrol .
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0.8962 0.9926 0.9999 Mononuclear leukocyte proteinglucocorticoid receptor binding characteristics and down-regulation in major depression .
0.8263 0.9989 0.9878 cell_typeMononuclear leukocyte glucocorticoid receptor binding characteristics and down-regulation in major depression .
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1.6993 10.9306 1.0000 To study whether this represents glucocorticoid ( GC ) resistance , [3H]-DEX-binding assays were used to measure, in vitro, the GC receptor affinity (1/Kd) and number ( Bmax ) in cell_typemononuclear leukocytes of 11 MDD patients and 15 control subjects .
1.6945 10.9924 1.0000 To study whether this represents glucocorticoid ( GC ) resistance , [3H]-DEX-binding assays were used to measure, in vitro, the proteinGC receptor affinity (1/Kd) and number ( Bmax ) in mononuclear leukocytes of 11 MDD patients and 15 control subjects .
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2.3889 20.1513 0.9999 DEX (1.0 mg orally) was administered to study in vivo proteinGC receptor down-regulation .
DEX (1.0 mg orally) was administered to study in proteinvivo GC receptor down-regulation .
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1.8272 10.1888 1.0000 Receptor number on the control day did not correlate significantly with the degree of proteinreceptor down-regulation , severity of depression or cortisol concentrations across all the subjects.
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1.5406 0.9983 10.6161 proteinRas-related GTP-binding proteins and leukocyte signal transduction .
Ras-related GTP-binding proteins and cell_typeleukocyte signal transduction .
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3.2651 10.9917 10.9762 Many aspects of leukocyte function are regulated by both heterotrimeric and proteinRas-related GTP-binding proteins , but there is little definite information about their roles in the specialized processes utilized by leukocytes for cell killing.
1.7246 10.3372 1.0000 Many aspects of leukocyte function are regulated by both heterotrimeric and Ras-related GTP-binding proteins , but there is little definite information about their roles in the specialized processes utilized by cell_typeleukocytes for cell killing.
0.8517 0.9995 1.0000 Many aspects of leukocyte function are regulated by both proteinheterotrimeric and Ras-related GTP-binding proteins , but there is little definite information about their roles in the specialized processes utilized by leukocytes for cell killing.
0.8237 1.0000 0.9999 Many aspects of cell_typeleukocyte function are regulated by both heterotrimeric and Ras-related GTP-binding proteins , but there is little definite information about their roles in the specialized processes utilized by leukocytes for cell killing.
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3.7422 20.4847 10.9898 Recent progress in understanding the regulation of the proteinphagocyte NADPH oxidase by the Rac GTP-binding proteins provides a basis for defining the operational characteristics of one such phagocyte system .
2.9969 20.1898 10.6271 Recent progress in understanding the regulation of the phagocyte NADPH oxidase by the proteinRac GTP-binding proteins provides a basis for defining the operational characteristics of one such phagocyte system .
1.3042 10.6559 0.9965 Recent progress in understanding the regulation of the phagocyte NADPH oxidase by the proteinRac GTP-binding proteins provides a basis for defining the operational characteristics of one such phagocyte system .
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2.2823 20.6550 1.0000 It is clear from various studies that the activity of the proteinNADPH oxidase can be modulated through the regulation of the GTP-GDP state of Rac .
2.2264 20.9231 0.9999 It is clear from various studies that the activity of the NADPH oxidase can be modulated through the regulation of the proteinGTP-GDP state of Rac .
1.6444 10.1025 1.0000 It is clear from various studies that the activity of the NADPH oxidase can be modulated through the regulation of the GTP-GDP state of proteinRac .
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2.4602 20.2688 1.0000 Proteins exist in leukocytes able to modify proteinGTP-binding protein function in this manner, and their activity may be regulated by signals generated on phagocyte stimulation .
0.8848 0.9999 1.0000 Proteins exist in cell_typeleukocytes able to modify GTP-binding protein function in this manner, and their activity may be regulated by signals generated on phagocyte stimulation .
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2.4546 20.0754 1.0000 Proteins of the proteinRas superfamily are likely to be involved in a variety of normal phagocyte functions through their ability to modulate the assembly of actin filaments , direct vesicle trafficking and fusion, and so forth.
2.3843 20.3345 1.0000 Proteins of the Ras superfamily are likely to be involved in a variety of normal phagocyte functions through their ability to modulate the assembly of proteinactin filaments , direct vesicle trafficking and fusion, and so forth.
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0.9754 1.0000 1.0000 proteinBSAP : a key regulator of B-cell development and differentiation .
BSAP : a key regulator of cell_typeB-cell development and differentiation .
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1.6797 10.5288 1.0000 B-cell-specific activator protein ( BSAP ) is a recently identified member of the Pax-gene family of transcription factors ; in the lymphoid system , proteinBSAP is produced only in B cells .
1.5274 10.4374 0.9999 B-cell-specific activator protein ( BSAP ) is a recently identified member of the Pax-gene family of proteintranscription factors ; in the lymphoid system , BSAP is produced only in B cells .
1.4367 20.5050 0.9997 B-cell-specific activator protein ( BSAP ) is a recently identified member of the Pax-gene family of transcription factors ; in the lymphoid system , BSAP is produced only in cell_typeB cells .
0.9696 1.0000 1.0000 B-cell-specific activator protein ( proteinBSAP ) is a recently identified member of the Pax-gene family of transcription factors ; in the lymphoid system , BSAP is produced only in B cells .
0.7952 0.9954 0.9993 proteinB-cell-specific activator protein ( BSAP ) is a recently identified member of the Pax-gene family of transcription factors ; in the lymphoid system , BSAP is produced only in B cells .
2.2054 20.9152 0.9999 B-cell-specific activator protein ( BSAP ) is a recently identified member of the proteinPax-gene family of transcription factors ; in the lymphoid system , BSAP is produced only in B cells .
B-cell-specific activator protein ( BSAP ) is a recently identified member of the DNAPax-gene family of transcription factors ; in the lymphoid system , BSAP is produced only in B cells .
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2.3138 20.8618 0.9999 Here, Markus Neurath, Eckhard Stuber and Warren Strober describe the molecular structure of BSAP and focus on the ability of this protein to regulate the expression of DNAB-cell-specific genes .
1.7177 10.5129 1.0000 Here, Markus Neurath, Eckhard Stuber and Warren Strober describe the molecular structure of proteinBSAP and focus on the ability of this protein to regulate the expression of B-cell-specific genes .
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1.7576 10.5260 1.0000 They propose that proteinBSAP is a key protein of B cells and that it not only influence B-cell development but also influences the balance between B-cell proliferation and immunoglobulin secretion at later stages of B-cell differentiation .
1.7300 10.9993 1.0000 They propose that BSAP is a key protein of B cells and that it not only influence B-cell development but also influences the balance between B-cell proliferation and proteinimmunoglobulin secretion at later stages of B-cell differentiation .
1.6711 10.9030 1.0000 They propose that BSAP is a key protein of cell_typeB cells and that it not only influence B-cell development but also influences the balance between B-cell proliferation and immunoglobulin secretion at later stages of B-cell differentiation .
0.5821 1.0000 0.9999 They propose that BSAP is a key protein of B cells and that it not only influence B-cell development but also influences the balance between cell_typeB-cell proliferation and immunoglobulin secretion at later stages of B-cell differentiation .
0.5788 1.0000 0.9999 They propose that BSAP is a key protein of B cells and that it not only influence B-cell development but also influences the balance between B-cell proliferation and immunoglobulin secretion at later stages of cell_typeB-cell differentiation .
They propose that BSAP is a proteinkey protein of B cells and that it not only influence B-cell development but also influences the balance between B-cell proliferation and immunoglobulin secretion at later stages of B-cell differentiation .
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3.8001 20.3268 10.9976 Down-regulation of NF-kappa B protein levels in cell_typeactivated human lymphocytes by 1,25-dihydroxyvitamin D3 [published erratum appears in Proc Natl Acad Sci U S A 1996 Jan 9;93(1):524]
2.3314 20.6535 0.9999 Down-regulation of proteinNF-kappa B protein levels in activated human lymphocytes by 1,25-dihydroxyvitamin D3 [published erratum appears in Proc Natl Acad Sci U S A 1996 Jan 9;93(1):524]
Down-regulation of proteinNF-kappa B protein levels in activated human lymphocytes by 1,25-dihydroxyvitamin D3 [published erratum appears in Proc Natl Acad Sci U S A 1996 Jan 9;93(1):524]
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3.1646 30.4033 10.5591 The effect of 1,25-dihydroxyvitamin D3 [ 1,25(OH)2)D3 ], a steroid hormone with immunomodulating properties, on proteinnuclear factor kappa B ( NF-kappa B ) proteins was examined in in vitro activated normal human lymphocytes by Western blot analysis .
0.9215 1.0000 0.9645 The effect of 1,25-dihydroxyvitamin D3 [ 1,25(OH)2)D3 ], a steroid hormone with immunomodulating properties, on nuclear factor kappa B ( proteinNF-kappa B ) proteins was examined in in vitro activated normal human lymphocytes by Western blot analysis .
7.8448 40.4567 20.8695 The effect of 1,25-dihydroxyvitamin D3 [ 1,25(OH)2)D3 ], a steroid hormone with immunomodulating properties, on nuclear factor kappa B ( NF-kappa B ) proteins was examined in cell_typein vitro activated normal human lymphocytes by Western blot analysis .
4.7446 30.8268 20.7641 The effect of 1,25-dihydroxyvitamin D3 [ 1,25(OH)2)D3 ], a steroid hormone with immunomodulating properties, on proteinnuclear factor kappa B ( NF-kappa B ) proteins was examined in in vitro activated normal human lymphocytes by Western blot analysis .
The effect of 1,25-dihydroxyvitamin D3 [ 1,25(OH)2)D3 ], a steroid hormone with immunomodulating properties, on nuclear factor kappa B ( NF-kappa B ) proteins was examined in cell_linein vitro activated normal human lymphocytes by Western blot analysis .
The effect of 1,25-dihydroxyvitamin D3 [ 1,25(OH)2)D3 ], a steroid hormone with immunomodulating properties, on nuclear factor kappa B ( NF-kappa B ) proteins was examined in in vitro activated normal cell_typehuman lymphocytes by Western blot analysis .
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3.5875 20.5709 10.7936 Over a 72-hr period of activation, the expression of the protein50-kDa NF-kappa B , p50 , and its precursor, p105 , was increased progressively.
1.6580 10.2298 1.0000 Over a 72-hr period of activation, the expression of the 50-kDa NF-kappa B , p50 , and its precursor, proteinp105 , was increased progressively.
0.9561 1.0000 1.0000 Over a 72-hr period of activation, the expression of the 50-kDa NF-kappa B , proteinp50 , and its precursor, p105 , was increased progressively.
0.7328 0.9999 0.9999 Over a 72-hr period of activation, the expression of the 50-kDa proteinNF-kappa B , p50 , and its precursor, p105 , was increased progressively.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5218 20.2963 1.0000 When cells were activated in the presence of 1,25(OH)2D3 , the levels of the proteinmature protein as well as its precursor were decreased.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8074 10.3989 1.0000 The effect of the hormone on the levels of proteinp50 was demonstrable in the cytosolic and nuclear compartments ; it required between 4 and 8 hr and was specific, as 25-hydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 were ineffective.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3152 20.2940 0.9999 Besides p50 , 1,25(OH)2D3 decreased the levels of another proteinNF-kappa B protein , namely c-rel .
1.5307 10.4238 1.0000 Besides proteinp50 , 1,25(OH)2D3 decreased the levels of another NF-kappa B protein , namely c-rel .
1.4021 10.6975 1.0000 Besides p50 , 1,25(OH)2D3 decreased the levels of another NF-kappa B protein , namely proteinc-rel .
1.7053 20.4423 0.8704 Besides p50 , 1,25(OH)2D3 decreased the levels of another proteinNF-kappa B protein , namely c-rel .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9366 20.4009 0.9849 In addition, 1,25(OH)2D3 decreased the abundance of a specific DNA-protein complex formed upon incubation of nuclear extracts from activated lymphocytes with a labeled proteinNF-kappa B DNA binding motif .
4.9814 20.7598 10.6323 In addition, 1,25(OH)2D3 decreased the abundance of a specific DNA-protein complex formed upon incubation of nuclear extracts from activated lymphocytes with a labeled DNANF-kappa B DNA binding motif .
1.4127 10.9640 0.9999 In addition, 1,25(OH)2D3 decreased the abundance of a specific proteinDNA-protein complex formed upon incubation of nuclear extracts from activated lymphocytes with a labeled NF-kappa B DNA binding motif .
1.3750 10.7701 0.9997 In addition, 1,25(OH)2D3 decreased the abundance of a specific DNA-protein complex formed upon incubation of nuclear extracts from cell_typeactivated lymphocytes with a labeled NF-kappa B DNA binding motif .
0.7054 1.0000 0.9999 In addition, 1,25(OH)2D3 decreased the abundance of a specific DNA-protein complex formed upon incubation of nuclear extracts from activated cell_typelymphocytes with a labeled NF-kappa B DNA binding motif .
In addition, 1,25(OH)2D3 decreased the abundance of a specific DNA-protein complex formed upon incubation of nuclear extracts from activated lymphocytes with a labeled proteinNF-kappa B DNA binding motif .
In addition, 1,25(OH)2D3 decreased the abundance of a proteinspecific DNA-protein complex formed upon incubation of nuclear extracts from activated lymphocytes with a labeled NF-kappa B DNA binding motif .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.2594 30.6000 10.7972 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the NF-kappa B binding sequence of the DNAimmunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
3.8255 20.7849 10.8755 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the DNANF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
2.9151 20.9866 10.4070 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the DNAchloramphenicol acetyltransferase reporter gene .
2.1720 30.6153 0.9800 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the proteinchloramphenicol acetyltransferase reporter gene .
2.0832 20.3331 1.0000 Further, 1,25(OH)2D3 inhibited the transcriptional activity of proteinNF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
1.8777 20.8271 0.9631 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the proteinNF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
1.4791 10.8928 0.9999 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in cell_lineJurkat cells transiently transfected with a construct containing four tandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
1.1557 0.9992 10.2052 Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four tandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase DNAreporter gene .
Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a construct containing four DNAtandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
Further, 1,25(OH)2D3 inhibited the transcriptional activity of NF-kappa B in Jurkat cells transiently transfected with a DNAconstruct containing four tandem repeats of the NF-kappa B binding sequence of the immunoglobulin kappa light chain gene linked to the chloramphenicol acetyltransferase reporter gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5431 10.7061 1.0000 These observations demonstrate directly that there is de novo synthesis of proteinNF-kappa B during human lymphocyte activation and suggest that this process is hormonally regulated.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0067 10.9118 10.2286 The DNAmyeloid zinc finger gene , MZF-1 , regulates the CD34 promoter in vitro.
1.9730 20.9693 1.0000 The myeloid zinc finger gene , MZF-1 , regulates the DNACD34 promoter in vitro.
0.9268 1.0000 1.0000 The myeloid zinc finger gene , DNAMZF-1 , regulates the CD34 promoter in vitro.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8590 30.3269 10.7508 MZF-1 is a C2H2 zinc finger gene encoding a proteinputative transcriptional regulator of myeloid differentiation .
3.6745 20.7879 10.6618 MZF-1 is a DNAC2H2 zinc finger gene encoding a putative transcriptional regulator of myeloid differentiation .
0.9361 0.9999 1.0000 DNAMZF-1 is a C2H2 zinc finger gene encoding a putative transcriptional regulator of myeloid differentiation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6504 10.7951 10.6653 The MZF-1 protein contains 13 proteinC2H2 zinc fingers arranged in bipartite DNA binding domains containing zinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
0.8076 1.0000 1.0000 The MZF-1 protein contains 13 C2H2 zinc fingers arranged in bipartite DNA binding domains containing zinc fingers through 4 and, in the proteincarboxy-terminus , 5 through 13.
0.7573 0.9988 0.9999 The MZF-1 protein contains 13 C2H2 zinc fingers arranged in bipartite DNA binding domains containing proteinzinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
4.3679 20.3177 10.7092 The MZF-1 protein contains 13 C2H2 zinc fingers arranged in proteinbipartite DNA binding domains containing zinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
1.3869 10.6411 1.0000 The proteinMZF-1 protein contains 13 C2H2 zinc fingers arranged in bipartite DNA binding domains containing zinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
1.3184 10.7916 0.9926 The proteinMZF-1 protein contains 13 C2H2 zinc fingers arranged in bipartite DNA binding domains containing zinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
The MZF-1 protein contains 13 C2H2 zinc fingers arranged in bipartite proteinDNA binding domains containing zinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
The DNAMZF-1 protein contains 13 C2H2 zinc fingers arranged in bipartite DNA binding domains containing zinc fingers through 4 and, in the carboxy-terminus , 5 through 13.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7560 20.9354 10.4363 We previously identified the DNADNA consensus binding site recognized by the two DNA binding domains .
3.7122 20.8799 10.7925 We previously identified the DNA consensus binding site recognized by the two proteinDNA binding domains .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.7963 20.9972 10.7395 To assess the transcription regulatory function of MZF-1 , the full-length MZF-1 coding region was fused to the proteinDNA binding domain of the yeast transactivator GAL4 .
0.9476 1.0000 1.0000 To assess the transcription regulatory function of MZF-1 , the full-length MZF-1 coding region was fused to the DNA binding domain of the yeast transactivator proteinGAL4 .
2.9358 20.7049 10.8481 To assess the transcription regulatory function of MZF-1 , the full-length DNAMZF-1 coding region was fused to the DNA binding domain of the yeast transactivator GAL4 .
1.8782 20.4769 0.9992 To assess the transcription regulatory function of MZF-1 , the full-length MZF-1 coding region was fused to the DNA binding domain of the proteinyeast transactivator GAL4 .
1.4155 10.7249 0.9972 To assess the transcription regulatory function of MZF-1 , the full-length proteinMZF-1 coding region was fused to the DNA binding domain of the yeast transactivator GAL4 .
1.3735 10.7473 1.0000 To assess the transcription regulatory function of proteinMZF-1 , the full-length MZF-1 coding region was fused to the DNA binding domain of the yeast transactivator GAL4 .
To assess the transcription regulatory function of DNAMZF-1 , the full-length MZF-1 coding region was fused to the DNA binding domain of the yeast transactivator GAL4 .
To assess the transcription regulatory function of MZF-1 , the full-length DNAMZF-1 coding region was fused to the DNA binding domain of the yeast transactivator GAL4 .
To assess the transcription regulatory function of MZF-1 , the full-length MZF-1 coding region was fused to the DNA binding domain of the proteinyeast transactivator GAL4 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7805 20.9331 10.6415 The expression vector was cotransfected with the DNAchloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
3.6270 30.2155 10.9630 The expression vector was cotransfected with the proteinchloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
3.5792 20.4165 10.9588 The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the DNAthymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
3.3919 20.5982 10.5810 The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and cell_lineJurkat cell lines .
2.9682 10.7007 10.7776 The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing DNAGAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
0.9035 1.0000 1.0000 The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , cell_line293 , K562 , and Jurkat cell lines .
0.8832 1.0000 1.0000 The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , cell_lineK562 , and Jurkat cell lines .
0.7738 0.9993 0.9999 The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into cell_lineNIH 3T3 , 293 , K562 , and Jurkat cell lines .
1.2938 10.6313 0.9998 The DNAexpression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the thymidine kinase promoter containing proteinGAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
The expression vector was cotransfected with the chloramphenicol acetyl transferase (CAT) reporter gene regulated by the proteinthymidine kinase promoter containing GAL4 DNA binding sites into NIH 3T3 , 293 , K562 , and Jurkat cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9263 20.4604 10.9779 MZF-1 represses CAT reporter gene expression via GAL4 binding sites in the cell_linenonhematopoietic cell lines NIH 3T3 and 293 .
2.6465 10.4126 10.3640 MZF-1 represses DNACAT reporter gene expression via GAL4 binding sites in the nonhematopoietic cell lines NIH 3T3 and 293 .
0.9130 1.0000 0.9999 MZF-1 represses CAT reporter gene expression via GAL4 binding sites in the nonhematopoietic cell lines NIH 3T3 and cell_line293 .
0.8228 0.9976 0.9994 MZF-1 represses CAT reporter gene expression via GAL4 binding sites in the nonhematopoietic cell lines cell_lineNIH 3T3 and 293 .
2.5232 10.9109 10.8327 MZF-1 represses CAT reporter gene expression via DNAGAL4 binding sites in the nonhematopoietic cell lines NIH 3T3 and 293 .
0.9500 1.0000 1.0000 proteinMZF-1 represses CAT reporter gene expression via GAL4 binding sites in the nonhematopoietic cell lines NIH 3T3 and 293 .
0.6313 1.0000 0.9999 MZF-1 represses CAT reporter gene expression via GAL4 binding sites in the nonhematopoietic cell lines NIH cell_line3T3 and 293 .
MZF-1 represses CAT reporter gene expression via proteinGAL4 binding sites in the nonhematopoietic cell lines NIH 3T3 and 293 .
DNAMZF-1 represses CAT reporter gene expression via GAL4 binding sites in the nonhematopoietic cell lines NIH 3T3 and 293 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3893 20.3329 10.7414 In contrast, MZF-1 activates DNACAT reporter gene expression in the hematopoietic cell lines K562 and Jurkat .
3.3545 20.1895 10.6465 In contrast, MZF-1 activates CAT reporter gene expression in the cell_linehematopoietic cell lines K562 and Jurkat .
0.9117 0.9999 0.9998 In contrast, MZF-1 activates CAT reporter gene expression in the hematopoietic cell lines cell_lineK562 and Jurkat .
0.9049 1.0000 1.0000 In contrast, MZF-1 activates CAT reporter gene expression in the hematopoietic cell lines K562 and cell_lineJurkat .
1.6729 10.0743 1.0000 In contrast, proteinMZF-1 activates CAT reporter gene expression in the hematopoietic cell lines K562 and Jurkat .
In contrast, DNAMZF-1 activates CAT reporter gene expression in the hematopoietic cell lines K562 and Jurkat .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0202 10.7998 10.9423 The DNAMZF-1 binding sites are present in the promoters of several genes expressed during myeloid differentiation , including the CD34 promoter .
2.0721 20.8282 0.9999 The MZF-1 binding sites are present in the promoters of several genes expressed during myeloid differentiation , including the DNACD34 promoter .
0.8956 1.0000 1.0000 The MZF-1 binding sites are present in the DNApromoters of several genes expressed during myeloid differentiation , including the CD34 promoter .
1.7931 20.7774 0.9782 The MZF-1 binding sites are present in the promoters of several genes expressed during myeloid differentiation , including the proteinCD34 promoter .
0.7735 0.9999 0.9954 The proteinMZF-1 binding sites are present in the promoters of several genes expressed during myeloid differentiation , including the CD34 promoter .
The MZF-1 binding sites are present in the promoters of several DNAgenes expressed during myeloid differentiation , including the CD34 promoter .
The DNAMZF-1 binding sites are present in the promoters of several genes expressed during myeloid differentiation , including the CD34 promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9874 1.0000 1.0000 proteinMZF-1 transcriptional regulation of this physiologically relevant promoter was assessed in both hematopoietic and nonhematopoietic cell lines .
MZF-1 transcriptional regulation of this physiologically relevant promoter was assessed in both hematopoietic and cell_linenonhematopoietic cell lines .
MZF-1 transcriptional regulation of this DNAphysiologically relevant promoter was assessed in both hematopoietic and nonhematopoietic cell lines .
DNAMZF-1 transcriptional regulation of this physiologically relevant promoter was assessed in both hematopoietic and nonhematopoietic cell lines .
MZF-1 transcriptional regulation of this physiologically relevant promoter was assessed in both cell_linehematopoietic and nonhematopoietic cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5162 20.4291 10.4423 Recombinant MZF-1 protein specifically binds to the DNAconsensus binding sites in the CD34 promoter in mobility shift assays .
2.1072 20.3030 1.0000 Recombinant MZF-1 protein specifically binds to the consensus binding sites in the DNACD34 promoter in mobility shift assays .
1.7965 20.4296 0.9871 Recombinant MZF-1 protein specifically binds to the consensus binding sites in the proteinCD34 promoter in mobility shift assays .
0.8972 0.9999 0.9975 Recombinant proteinMZF-1 protein specifically binds to the consensus binding sites in the CD34 promoter in mobility shift assays .
0.5160 0.9920 1.0000 Recombinant proteinMZF-1 protein specifically binds to the consensus binding sites in the CD34 promoter in mobility shift assays .
proteinRecombinant MZF-1 protein specifically binds to the consensus binding sites in the CD34 promoter in mobility shift assays .
Recombinant DNAMZF-1 protein specifically binds to the consensus binding sites in the CD34 promoter in mobility shift assays .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5668 20.4770 10.8679 MZF-1 expression vectors were cotransfected with the DNAluciferase reporter plasmids regulated by the CD34 promoter into both nonhematopoietic and hematopoietic cell lines .
1.3332 10.9751 0.9999 MZF-1 expression vectors were cotransfected with the luciferase reporter plasmids regulated by the DNACD34 promoter into both nonhematopoietic and hematopoietic cell lines .
2.5640 10.6851 10.3048 MZF-1 expression vectors were cotransfected with the luciferase reporter plasmids regulated by the CD34 promoter into both nonhematopoietic and cell_linehematopoietic cell lines .
1.4611 0.9926 10.6429 DNAMZF-1 expression vectors were cotransfected with the luciferase reporter plasmids regulated by the CD34 promoter into both nonhematopoietic and hematopoietic cell lines .
0.8587 1.0000 0.9927 proteinMZF-1 expression vectors were cotransfected with the luciferase reporter plasmids regulated by the CD34 promoter into both nonhematopoietic and hematopoietic cell lines .
DNAMZF-1 expression vectors were cotransfected with the luciferase reporter plasmids regulated by the CD34 promoter into both nonhematopoietic and hematopoietic cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4063 20.6282 10.6195 As with the heterologous DNA binding domain , MZF-1 represses reporter gene expression in cell_linenonhematopoietic cell lines and activates expression in hematopoietic cell lines .
3.3087 20.9135 10.5486 As with the heterologous DNA binding domain , MZF-1 represses reporter gene expression in nonhematopoietic cell lines and activates expression in cell_linehematopoietic cell lines .
3.5835 20.9226 10.6945 As with the proteinheterologous DNA binding domain , MZF-1 represses reporter gene expression in nonhematopoietic cell lines and activates expression in hematopoietic cell lines .
0.9489 1.0000 1.0000 As with the heterologous DNA binding domain , proteinMZF-1 represses reporter gene expression in nonhematopoietic cell lines and activates expression in hematopoietic cell lines .
As with the heterologous proteinDNA binding domain , MZF-1 represses reporter gene expression in nonhematopoietic cell lines and activates expression in hematopoietic cell lines .
As with the heterologous DNA binding domain , MZF-1 represses DNAreporter gene expression in nonhematopoietic cell lines and activates expression in hematopoietic cell lines .
As with the heterologous DNA binding domain , DNAMZF-1 represses reporter gene expression in nonhematopoietic cell lines and activates expression in hematopoietic cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1302 20.3582 10.7424 Activation of CD34 expression in cell_linehematopoietic cell lines is dependent on the presence of intact MZF-1 binding sites .
2.8950 20.4870 10.6426 Activation of CD34 expression in hematopoietic cell lines is dependent on the presence of intact DNAMZF-1 binding sites .
1.4171 10.7658 1.0000 Activation of proteinCD34 expression in hematopoietic cell lines is dependent on the presence of intact MZF-1 binding sites .
1.1823 10.5083 0.9936 Activation of CD34 expression in hematopoietic cell lines is dependent on the presence of intact proteinMZF-1 binding sites .
Activation of CD34 expression in hematopoietic cell lines is dependent on the presence of intact DNAMZF-1 binding sites .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1050 20.2854 1.0000 The cell type-specific regulation of the DNACD34 promoter by MZF-1 suggests the presence of tissue-specific regulators/adapters or differential MZF-1 modifications that determine MZF-1 transcriptional regulatory function .
2.1244 20.4755 0.9999 The cell type-specific regulation of the CD34 promoter by MZF-1 suggests the presence of proteintissue-specific regulators/adapters or differential MZF-1 modifications that determine MZF-1 transcriptional regulatory function .
2.0253 20.3871 0.9905 The cell type-specific regulation of the proteinCD34 promoter by MZF-1 suggests the presence of tissue-specific regulators/adapters or differential MZF-1 modifications that determine MZF-1 transcriptional regulatory function .
1.6040 10.1808 1.0000 The cell type-specific regulation of the CD34 promoter by MZF-1 suggests the presence of tissue-specific regulators/adapters or differential proteinMZF-1 modifications that determine MZF-1 transcriptional regulatory function .
0.8584 1.0000 1.0000 The cell type-specific regulation of the CD34 promoter by proteinMZF-1 suggests the presence of tissue-specific regulators/adapters or differential MZF-1 modifications that determine MZF-1 transcriptional regulatory function .
0.8023 1.0000 1.0000 The cell type-specific regulation of the CD34 promoter by MZF-1 suggests the presence of tissue-specific regulators/adapters or differential MZF-1 modifications that determine proteinMZF-1 transcriptional regulatory function .
The cell type-specific regulation of the CD34 promoter by MZF-1 suggests the presence of tissue-specific regulators/adapters or differential DNAMZF-1 modifications that determine MZF-1 transcriptional regulatory function .
The cell type-specific regulation of the CD34 promoter by MZF-1 suggests the presence of tissue-specific regulators/adapters or differential MZF-1 modifications that determine DNAMZF-1 transcriptional regulatory function .
The cell type-specific regulation of the CD34 promoter by DNAMZF-1 suggests the presence of tissue-specific regulators/adapters or differential MZF-1 modifications that determine MZF-1 transcriptional regulatory function .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2526 30.0859 10.9792 The murine BCL6 gene is induced in activated lymphocytes as an DNAimmediate early gene .
0.8001 1.0000 0.9999 The murine BCL6 gene is induced in activated cell_typelymphocytes as an immediate early gene .
0.6605 0.8676 0.9979 The DNAmurine BCL6 gene is induced in activated lymphocytes as an immediate early gene .
The murine DNABCL6 gene is induced in activated lymphocytes as an immediate early gene .
The murine BCL6 gene is induced in cell_typeactivated lymphocytes as an immediate early gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0082 20.7960 10.9372 The chromosomal translocation involving 3q27 is often detected in cell_typehuman B-cell lymphomas , especially diffuse lymphomas with a large-cell component .
1.6909 10.8479 1.0000 The chromosomal translocation involving DNA3q27 is often detected in human B-cell lymphomas , especially diffuse lymphomas with a large-cell component .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5956 10.8242 1.0000 The DNABCL6 gene has been isolated from the chromosomal breakpoint in these lymphomas .
1.8549 20.1690 1.0000 The BCL6 gene has been isolated from the DNAchromosomal breakpoint in these lymphomas .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.4738 30.2635 10.9017 Here we cloned the murine BCL6 (mBCL6) cDNA from the muscle cDNA library using the DNAhuman BCL6 (hBCL6) cDNA as a probe.
4.4504 20.9042 10.9421 Here we cloned the DNAmurine BCL6 (mBCL6) cDNA from the muscle cDNA library using the human BCL6 (hBCL6) cDNA as a probe.
Here we cloned the murine BCL6 (mBCL6) cDNA from the DNAmuscle cDNA library using the human BCL6 (hBCL6) cDNA as a probe.
Here we cloned the proteinmurine BCL6 (mBCL6) cDNA from the muscle cDNA library using the human BCL6 (hBCL6) cDNA as a probe.
Here we cloned the murine BCL6 (mBCL6) cDNA from the muscle cDNA library using the proteinhuman BCL6 (hBCL6) cDNA as a probe.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.3601 10.9096 1.0000 The predicted amino acid sequence was 95% identical to that of proteinhBCL6 .
4.1643 20.4346 10.9622 The predicted proteinamino acid sequence was 95% identical to that of hBCL6 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3881 20.9212 1.0000 It contains six repeats of the proteinKruppel-like zinc-finger motif that are completely identical to those of hBCL6 , indicating that the BCL6 gene is well conserved between humans and mice .
1.5614 10.6621 1.0000 It contains six repeats of the Kruppel-like zinc-finger motif that are completely identical to those of proteinhBCL6 , indicating that the BCL6 gene is well conserved between humans and mice .
1.4738 20.8023 1.0000 It contains six repeats of the Kruppel-like zinc-finger motif that are completely identical to those of hBCL6 , indicating that the DNABCL6 gene is well conserved between humans and mice .
1.3983 20.8399 0.9892 It contains six repeats of the Kruppel-like zinc-finger motif that are completely identical to those of hBCL6 , indicating that the proteinBCL6 gene is well conserved between humans and mice .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2595 20.3658 1.0000 Expression of the DNAmBCL6 gene was ubiquitously detected in adult mouse tissues including lymphatic organs .
2.0463 20.3073 0.9919 Expression of the proteinmBCL6 gene was ubiquitously detected in adult mouse tissues including lymphatic organs .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7667 10.7387 1.0000 Furthermore, it was induced in cell_typelymphocytes activated with phorbol ester and Ca2+ ionophore within 30 min after stimulation.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9419 20.1515 0.9998 These results suggest that BCL6 plays a role in cell_typeactivated lymphocytes as an immediate early gene.
1.4610 10.8433 1.0000 These results suggest that proteinBCL6 plays a role in activated lymphocytes as an immediate early gene.
0.8428 1.0000 0.9999 These results suggest that BCL6 plays a role in activated cell_typelymphocytes as an immediate early gene.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7804 20.7795 0.9986 The role of proteinBSAP ( Pax-5 ) in B-cell development .
0.9028 0.9999 0.9998 The role of BSAP ( proteinPax-5 ) in B-cell development .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.2403 30.1563 10.6722 In this manner, the paired box containing gene Pax-5 , encoding the proteinB cell specific transcription factor BSAP , has been shown to play a key role in early B lymphopoiesis .
3.2644 30.8376 10.3615 In this manner, the DNApaired box containing gene Pax-5 , encoding the B cell specific transcription factor BSAP , has been shown to play a key role in early B lymphopoiesis .
0.9715 0.9999 1.0000 In this manner, the paired box containing gene Pax-5 , encoding the B cell specific transcription factor proteinBSAP , has been shown to play a key role in early B lymphopoiesis .
0.9454 0.9997 1.0000 In this manner, the paired box containing gene DNAPax-5 , encoding the B cell specific transcription factor BSAP , has been shown to play a key role in early B lymphopoiesis .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6982 30.0149 0.9325 Other experimental strategies have implicated BSAP in the control of cell proliferation , isotype switching and transcription of the proteinimmunoglobulin heavy-chain gene at late stages of B-cell differentiation .
2.1852 20.9727 0.9999 Other experimental strategies have implicated BSAP in the control of cell proliferation , isotype switching and transcription of the DNAimmunoglobulin heavy-chain gene at late stages of B-cell differentiation .
1.6232 10.8656 1.0000 Other experimental strategies have implicated proteinBSAP in the control of cell proliferation , isotype switching and transcription of the immunoglobulin heavy-chain gene at late stages of B-cell differentiation .
0.6834 0.9999 0.9998 Other experimental strategies have implicated BSAP in the control of cell proliferation , isotype switching and transcription of the immunoglobulin heavy-chain gene at late stages of cell_typeB-cell differentiation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3374 20.9945 10.2572 The DNA-binding properties of two heat shock factors , HSF1 and HSF3 , are induced in the cell_lineavian erythroblast cell line HD6 .
0.9399 1.0000 1.0000 The DNA-binding properties of two heat shock factors , HSF1 and proteinHSF3 , are induced in the avian erythroblast cell line HD6 .
0.9106 1.0000 1.0000 The DNA-binding properties of two heat shock factors , proteinHSF1 and HSF3 , are induced in the avian erythroblast cell line HD6 .
0.9071 0.9990 0.9998 The DNA-binding properties of two heat shock factors , HSF1 and HSF3 , are induced in the avian erythroblast cell line cell_lineHD6 .
4.0031 30.2897 20.0847 The DNA-binding properties of two heat shock factors , HSF1 and HSF3 , are induced in the cell_lineavian erythroblast cell line HD6 .
3.1405 20.5221 10.5332 The DNA-binding properties of two proteinheat shock factors , HSF1 and HSF3 , are induced in the avian erythroblast cell line HD6 .
The DNA-binding properties of proteintwo heat shock factors , HSF1 and HSF3 , are induced in the avian erythroblast cell line HD6 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.8478 30.3131 20.4121 Avian cells express three DNAheat shock transcription factor ( HSF ) genes corresponding to a novel factor , HSF3 , and homologs of mouse and human HSF1 and HSF2 .
2.5892 40.4744 10.3972 Avian cells express three proteinheat shock transcription factor ( HSF ) genes corresponding to a novel factor , HSF3 , and homologs of mouse and human HSF1 and HSF2 .
1.7134 10.4470 1.0000 Avian cells express three heat shock transcription factor ( HSF ) genes corresponding to a novel factor , proteinHSF3 , and homologs of mouse and human HSF1 and HSF2 .
1.1132 10.2503 1.0000 Avian cells express three heat shock transcription factor ( HSF ) genes corresponding to a proteinnovel factor , HSF3 , and homologs of mouse and human HSF1 and HSF2 .
0.9592 1.0000 0.9860 Avian cells express three heat shock transcription factor ( proteinHSF ) genes corresponding to a novel factor , HSF3 , and homologs of mouse and human HSF1 and HSF2 .
0.8458 1.0000 1.0000 Avian cells express three heat shock transcription factor ( HSF ) genes corresponding to a novel factor , HSF3 , and homologs of mouse and human HSF1 and proteinHSF2 .
Avian cells express three heat shock transcription factor ( HSF ) genes corresponding to a novel factor , HSF3 , and homologs of mouse and human proteinHSF1 and HSF2 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7149 10.6728 1.0000 Analysis of the biochemical and cell biological properties of these HSFs reveals that proteinHSF3 has properties in common with both HSF1 and HSF2 and yet has features which are distinct from both.
1.6985 10.7443 1.0000 Analysis of the biochemical and cell biological properties of these HSFs reveals that HSF3 has properties in common with both proteinHSF1 and HSF2 and yet has features which are distinct from both.
1.6108 10.8744 1.0000 Analysis of the biochemical and cell biological properties of these proteinHSFs reveals that HSF3 has properties in common with both HSF1 and HSF2 and yet has features which are distinct from both.
0.9459 1.0000 1.0000 Analysis of the biochemical and cell biological properties of these HSFs reveals that HSF3 has properties in common with both HSF1 and proteinHSF2 and yet has features which are distinct from both.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6976 20.6325 10.9675 HSF3 is constitutively expressed in the erythroblast cell line HD6 , the cell_linelymphoblast cell line MSB , and embryo fibroblasts , and yet its DNA-binding activity is induced only upon exposure of HD6 cells to heat shock.
4.6395 20.9904 10.4224 HSF3 is constitutively expressed in the cell_lineerythroblast cell line HD6 , the lymphoblast cell line MSB , and embryo fibroblasts , and yet its DNA-binding activity is induced only upon exposure of HD6 cells to heat shock.
0.9643 1.0000 1.0000 proteinHSF3 is constitutively expressed in the erythroblast cell line HD6 , the lymphoblast cell line MSB , and embryo fibroblasts , and yet its DNA-binding activity is induced only upon exposure of HD6 cells to heat shock.
2.1034 20.7446 0.9999 HSF3 is constitutively expressed in the erythroblast cell line HD6 , the lymphoblast cell line MSB , and embryo fibroblasts , and yet its DNA-binding activity is induced only upon exposure of cell_lineHD6 cells to heat shock.
1.9629 20.0864 0.9996 HSF3 is constitutively expressed in the erythroblast cell line HD6 , the lymphoblast cell line MSB , and cell_typeembryo fibroblasts , and yet its DNA-binding activity is induced only upon exposure of HD6 cells to heat shock.
HSF3 is constitutively expressed in the erythroblast cell line HD6 , the lymphoblast cell line MSB , and cell_lineembryo fibroblasts , and yet its DNA-binding activity is induced only upon exposure of HD6 cells to heat shock.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2129 20.3586 0.9999 Acquisition of HSF3 DNA-binding activity in HD6 cells is accompanied by oligomerization from a proteinnon-DNA-binding dimer to a DNA-binding trimer , whereas the effect of heat shock on HSF1 is oligomerization of an inert monomer to a DNA-binding trimer .
1.5779 10.5109 1.0000 Acquisition of HSF3 DNA-binding activity in HD6 cells is accompanied by oligomerization from a non-DNA-binding dimer to a DNA-binding trimer , whereas the effect of heat shock on proteinHSF1 is oligomerization of an inert monomer to a DNA-binding trimer .
1.5004 10.9110 0.9999 Acquisition of HSF3 DNA-binding activity in cell_lineHD6 cells is accompanied by oligomerization from a non-DNA-binding dimer to a DNA-binding trimer , whereas the effect of heat shock on HSF1 is oligomerization of an inert monomer to a DNA-binding trimer .
1.4756 10.9400 0.9999 Acquisition of HSF3 DNA-binding activity in HD6 cells is accompanied by oligomerization from a non-DNA-binding dimer to a proteinDNA-binding trimer , whereas the effect of heat shock on HSF1 is oligomerization of an inert monomer to a DNA-binding trimer .
1.4753 10.6386 1.0000 Acquisition of proteinHSF3 DNA-binding activity in HD6 cells is accompanied by oligomerization from a non-DNA-binding dimer to a DNA-binding trimer , whereas the effect of heat shock on HSF1 is oligomerization of an inert monomer to a DNA-binding trimer .
1.4591 10.8418 0.9999 Acquisition of HSF3 DNA-binding activity in HD6 cells is accompanied by oligomerization from a non-DNA-binding dimer to a DNA-binding trimer , whereas the effect of heat shock on HSF1 is oligomerization of an inert monomer to a proteinDNA-binding trimer .
Acquisition of HSF3 DNA-binding activity in HD6 cells is accompanied by oligomerization from a non-DNA-binding dimer to a DNA-binding trimer , whereas the effect of heat shock on HSF1 is oligomerization of an proteininert monomer to a DNA-binding trimer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5022 10.9360 1.0000 Induction of proteinHSF3 DNA-binding activity is delayed compared with that of HSF1 .
1.3722 10.9664 1.0000 Induction of HSF3 DNA-binding activity is delayed compared with that of proteinHSF1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3333 20.0531 1.0000 As occurs for proteinHSF1 , heat shock leads to the translocation of HSF3 to the nucleus.
1.5812 10.6708 1.0000 As occurs for HSF1 , heat shock leads to the translocation of proteinHSF3 to the nucleus.
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.3595 30.0470 10.3494 HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a DNAheat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a GAL4 reporter construct .
4.6176 30.0254 10.8747 HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a proteinchimeric GAL4 -HSF3 protein on a GAL4 reporter construct .
3.2699 20.8222 10.8844 HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a DNAGAL4 reporter construct .
1.9963 20.0772 1.0000 HSF exhibits the properties of a proteintranscriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a GAL4 reporter construct .
1.5200 10.1266 1.0000 HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed proteinHSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a GAL4 reporter construct .
0.5312 1.0000 0.9492 HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 protein-HSF3 protein on a GAL4 reporter construct .
0.8837 1.0000 1.0000 proteinHSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a GAL4 reporter construct .
HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric proteinGAL4 -HSF3 protein on a GAL4 reporter construct .
HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of transiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a proteinGAL4 reporter construct .
HSF exhibits the properties of a transcriptional activator , as judged from the stimulatory activity of proteintransiently overexpressed HSF3 measured by using a heat shock element-containing reporter construct and as independently assayed by the activity of a chimeric GAL4 -HSF3 protein on a GAL4 reporter construct .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.8864 1.0000 1.0000 These results reveal that proteinHSF3 is negatively regulated in avian cells and acquires DNA-binding activity in certain cells upon heat shock .
These results reveal that HSF3 is negatively regulated in cell_typeavian cells and acquires DNA-binding activity in certain cells upon heat shock .
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3.3852 20.2467 10.5259 Direct demonstration of NFATp dephosphorylation and nuclear localization in activated HT-2 cells using a specific proteinNFATp polyclonal antibody .
1.3487 10.5081 1.0000 Direct demonstration of proteinNFATp dephosphorylation and nuclear localization in activated HT-2 cells using a specific NFATp polyclonal antibody .
1.2668 10.3005 0.9964 Direct demonstration of NFATp dephosphorylation and nuclear localization in activated HT-2 cells using a specific proteinNFATp polyclonal antibody .
Direct demonstration of NFATp dephosphorylation and nuclear localization in cell_lineactivated HT-2 cells using a specific NFATp polyclonal antibody .
Direct demonstration of NFATp dephosphorylation and nuclear localization in activated cell_lineHT-2 cells using a specific NFATp polyclonal antibody .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5540 0.9988 20.7060 proteinNuclear factor of activated T cells ( NFAT ) regulates transcription of a number of cytokine genes , and NFAT DNA binding activity is stimulated following T cell activation .
1.5266 10.1391 1.0000 Nuclear factor of activated T cells ( NFAT ) regulates transcription of a number of cytokine genes , and proteinNFAT DNA binding activity is stimulated following T cell activation .
0.9761 1.0000 1.0000 Nuclear factor of activated T cells ( proteinNFAT ) regulates transcription of a number of cytokine genes , and NFAT DNA binding activity is stimulated following T cell activation .
2.0128 20.5638 0.9999 Nuclear factor of activated T cells ( NFAT ) regulates transcription of a number of DNAcytokine genes , and NFAT DNA binding activity is stimulated following T cell activation .
Nuclear factor of activated T cells ( NFAT ) regulates transcription of a number of proteincytokine genes , and NFAT DNA binding activity is stimulated following T cell activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6045 10.7318 1.0000 Several lines of evidence have suggested that proteinNFAT is a substrate for calcineurin , a serine/threonine phosphatase .
1.4997 10.7551 1.0000 Several lines of evidence have suggested that NFAT is a substrate for proteincalcineurin , a serine/threonine phosphatase .
1.4147 10.3013 0.9999 Several lines of evidence have suggested that NFAT is a substrate for calcineurin , a proteinserine/threonine phosphatase .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.1605 10.5388 0.9999 Using a polyclonal antibody to proteinmurine NFATp , Western blot analysis of various mouse tissues demonstrated that the 110-130-kDa NFATp protein was highly expressed in thymus and spleen .
0.9263 1.0000 0.9891 Using a polyclonal antibody to murine NFATp , Western blot analysis of various mouse tissues demonstrated that the 110-130-kDa proteinNFATp protein was highly expressed in thymus and spleen .
0.9116 1.0000 1.0000 Using a polyclonal antibody to murine proteinNFATp , Western blot analysis of various mouse tissues demonstrated that the 110-130-kDa NFATp protein was highly expressed in thymus and spleen .
2.3411 20.9259 0.9999 Using a polyclonal antibody to murine NFATp , Western blot analysis of various mouse tissues demonstrated that the protein110-130-kDa NFATp protein was highly expressed in thymus and spleen .
1.9800 20.5329 0.9999 Using a proteinpolyclonal antibody to murine NFATp , Western blot analysis of various mouse tissues demonstrated that the 110-130-kDa NFATp protein was highly expressed in thymus and spleen .
Using a polyclonal antibody to murine NFATp , Western blot analysis of various mouse tissues demonstrated that the 110-130-kDa proteinNFATp protein was highly expressed in thymus and spleen .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5737 10.0859 1.0000 Treatment of immunoprecipitated NFATp from untreated HT-2 cells with calcineurin resulted in the dephosphorylation of NFATp , demonstrating that proteinNFATp is an in vitro substrate for calcineurin .
1.4988 10.4673 1.0000 Treatment of immunoprecipitated NFATp from untreated HT-2 cells with calcineurin resulted in the dephosphorylation of proteinNFATp , demonstrating that NFATp is an in vitro substrate for calcineurin .
1.4568 10.8854 1.0000 Treatment of immunoprecipitated NFATp from untreated HT-2 cells with calcineurin resulted in the dephosphorylation of NFATp , demonstrating that NFATp is an in vitro substrate for proteincalcineurin .
0.9061 1.0000 1.0000 Treatment of immunoprecipitated NFATp from untreated HT-2 cells with proteincalcineurin resulted in the dephosphorylation of NFATp , demonstrating that NFATp is an in vitro substrate for calcineurin .
0.9030 1.0000 1.0000 Treatment of immunoprecipitated proteinNFATp from untreated HT-2 cells with calcineurin resulted in the dephosphorylation of NFATp , demonstrating that NFATp is an in vitro substrate for calcineurin .
3.1106 10.5548 10.8765 Treatment of immunoprecipitated NFATp from cell_lineuntreated HT-2 cells with calcineurin resulted in the dephosphorylation of NFATp , demonstrating that NFATp is an in vitro substrate for calcineurin .
1.9857 20.5340 0.9998 Treatment of proteinimmunoprecipitated NFATp from untreated HT-2 cells with calcineurin resulted in the dephosphorylation of NFATp , demonstrating that NFATp is an in vitro substrate for calcineurin .
Treatment of immunoprecipitated NFATp from untreated cell_lineHT-2 cells with calcineurin resulted in the dephosphorylation of NFATp , demonstrating that NFATp is an in vitro substrate for calcineurin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9375 20.6200 10.8286 NFATp immunoprecipitated from cell_line32P-labeled HT-2 cells migrated as an approximately 120-kDa protein that was localized to the cytosol of the cells.
0.9700 1.0000 1.0000 proteinNFATp immunoprecipitated from 32P-labeled HT-2 cells migrated as an approximately 120-kDa protein that was localized to the cytosol of the cells.
2.1691 20.5180 1.0000 NFATp immunoprecipitated from 32P-labeled HT-2 cells migrated as an approximately protein120-kDa protein that was localized to the cytosol of the cells.
NFATp immunoprecipitated from 32P-labeled cell_lineHT-2 cells migrated as an approximately 120-kDa protein that was localized to the cytosol of the cells.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6512 10.9664 1.0000 Treatment of the cells with ionomycin resulted in a decrease in the molecular weight of proteinNFATp and a loss of 32P , consistent with NFATp dephosphorylation .
1.6506 10.5120 1.0000 Treatment of the cells with ionomycin resulted in a decrease in the molecular weight of NFATp and a loss of 32P , consistent with proteinNFATp dephosphorylation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6606 10.9432 1.0000 The dephosphorylation of proteinNFATp was accompanied by localization of the protein to the nuclear fraction .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6523 10.6311 1.0000 Both of these events were blocked by preincubation of the cells with FK506 , a calcineurin inhibitor , consistent with the hypothesis that proteinNFATp is a calcineurin substrate in cells.
1.5909 10.4345 1.0000 Both of these events were blocked by preincubation of the cells with FK506 , a proteincalcineurin inhibitor , consistent with the hypothesis that NFATp is a calcineurin substrate in cells.
1.5004 10.5621 0.9937 Both of these events were blocked by preincubation of the cells with FK506 , a calcineurin inhibitor , consistent with the hypothesis that NFATp is a proteincalcineurin substrate in cells.
1.5452 10.6312 0.9999 Both of these events were blocked by preincubation of the cells with FK506 , a calcineurin inhibitor , consistent with the hypothesis that NFATp is a proteincalcineurin substrate in cells.
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.2584 30.1920 10.9784 Activation and expression of the nuclear factors of activated T cells , NFATp and NFATc , in cell_typehuman natural killer cells : regulation upon CD16 ligand binding .
0.9515 1.0000 1.0000 Activation and expression of the nuclear factors of activated T cells , proteinNFATp and NFATc , in human natural killer cells : regulation upon CD16 ligand binding .
0.9460 1.0000 1.0000 Activation and expression of the nuclear factors of activated T cells , NFATp and proteinNFATc , in human natural killer cells : regulation upon CD16 ligand binding .
0.7770 1.0000 1.0000 Activation and expression of the nuclear factors of activated T cells , NFATp and NFATc , in human natural killer cells : regulation upon proteinCD16 ligand binding .
6.9409 30.9905 20.6418 Activation and expression of the proteinnuclear factors of activated T cells , NFATp and NFATc , in human natural killer cells : regulation upon CD16 ligand binding .
Activation and expression of the proteinnuclear factors of activated T cells , NFATp and NFATc , in human natural killer cells : regulation upon CD16 ligand binding .
Activation and expression of the nuclear factors of cell_typeactivated T cells , NFATp and NFATc , in human natural killer cells : regulation upon CD16 ligand binding .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6682 20.9372 10.7439 The putative factors that couple the signal transduction from surface receptors to the activation of cytokine synthesis in cell_typenatural killer (NK) cells have not been elucidated.
1.5888 10.1756 1.0000 The putative factors that couple the signal transduction from surface receptors to the activation of proteincytokine synthesis in natural killer (NK) cells have not been elucidated.
2.0307 20.7074 0.9999 The putative factors that couple the signal transduction from proteinsurface receptors to the activation of cytokine synthesis in natural killer (NK) cells have not been elucidated.
0.5248 0.9751 0.9999 The proteinputative factors that couple the signal transduction from surface receptors to the activation of cytokine synthesis in natural killer (NK) cells have not been elucidated.
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.2208 20.5860 20.9552 We report here that the nuclear factor of activated T cells ( NFATp ), a proteincyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of cytokine genes in human NK cells .
1.3108 10.1006 0.9947 We report here that the nuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of cytokine genes in cell_typehuman NK cells .
0.9650 1.0000 1.0000 We report here that the nuclear factor of activated T cells ( proteinNFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of cytokine genes in human NK cells .
0.9100 1.0000 1.0000 We report here that the nuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates proteinCD16 -induced activation of cytokine genes in human NK cells .
0.7860 0.9999 1.0000 We report here that the nuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several proteincytokines , mediates CD16 -induced activation of cytokine genes in human NK cells .
6.9784 30.9563 20.8680 We report here that the proteinnuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of cytokine genes in human NK cells .
2.0105 20.6346 0.9998 We report here that the nuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of DNAcytokine genes in human NK cells .
We report here that the nuclear factor of cell_typeactivated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of cytokine genes in human NK cells .
We report here that the proteinnuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of cytokine genes in human NK cells .
We report here that the nuclear factor of activated T cells ( NFATp ), a cyclosporin A ( CsA )-sensitive factor that regulates the transcription of several cytokines , mediates CD16 -induced activation of proteincytokine genes in human NK cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1196 10.6773 10.5322 CD16 ( proteinFc gamma RIIIA )-induced expression of cytokine mRNA in NK cells occurs via a CsA -sensitive and Ca(2+)-dependent mechanism .
1.5673 10.7457 0.9999 CD16 ( Fc gamma RIIIA )-induced expression of RNAcytokine mRNA in NK cells occurs via a CsA -sensitive and Ca(2+)-dependent mechanism .
1.4880 10.7579 0.9998 CD16 ( Fc gamma RIIIA )-induced expression of cytokine mRNA in cell_typeNK cells occurs via a CsA -sensitive and Ca(2+)-dependent mechanism .
0.9619 1.0000 1.0000 proteinCD16 ( Fc gamma RIIIA )-induced expression of cytokine mRNA in NK cells occurs via a CsA -sensitive and Ca(2+)-dependent mechanism .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7720 10.0198 1.0000 Stimulation of NK cells with proteinCD16 ligands induces NFAT -like DNA binding activity in the nuclear extracts from these cells, as detected in electrophoretic mobility shift assays .
1.6216 10.9232 0.9999 Stimulation of cell_typeNK cells with CD16 ligands induces NFAT -like DNA binding activity in the nuclear extracts from these cells, as detected in electrophoretic mobility shift assays .
0.9480 1.0000 1.0000 Stimulation of NK cells with CD16 ligands induces proteinNFAT -like DNA binding activity in the nuclear extracts from these cells, as detected in electrophoretic mobility shift assays .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2015 20.1394 0.9999 NK cell NFAT is present in the cytosol of cell_typenonstimulated cells , migrates to the nucleus upon stimulation, and can associate with AP-1 .
1.7289 0.9989 10.7045 proteinNK cell NFAT is present in the cytosol of nonstimulated cells , migrates to the nucleus upon stimulation, and can associate with AP-1 .
1.5046 10.9597 1.0000 NK cell NFAT is present in the cytosol of nonstimulated cells , migrates to the nucleus upon stimulation, and can associate with proteinAP-1 .
0.9511 1.0000 1.0000 NK cell proteinNFAT is present in the cytosol of nonstimulated cells , migrates to the nucleus upon stimulation, and can associate with AP-1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6242 10.6334 1.0000 Two distinct molecules, proteinNFATp and NFATc , have been reported to mediate NFAT activity .
1.5045 10.9764 1.0000 Two distinct molecules, NFATp and NFATc , have been reported to mediate proteinNFAT activity .
0.8877 1.0000 1.0000 Two distinct molecules, NFATp and proteinNFATc , have been reported to mediate NFAT activity .
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2.4362 20.5471 0.9999 The results of supershift assays using NFATp- and NFATc- specific antibodies indicate that NK cell activation early after CD16 ligand binding involves primarily, if not exclusively, NFATp , and Western blot analysis shows that this has the same electrophoretic mobility (approximately 120 kD) as that of cell_typeT lymphocytes .
1.7659 10.3783 1.0000 The results of supershift assays using NFATp- and NFATc- specific antibodies indicate that NK cell activation early after CD16 ligand binding involves primarily, if not exclusively, proteinNFATp , and Western blot analysis shows that this has the same electrophoretic mobility (approximately 120 kD) as that of T lymphocytes .
0.8787 1.0000 1.0000 The results of supershift assays using NFATp- and NFATc- specific antibodies indicate that NK cell activation early after proteinCD16 ligand binding involves primarily, if not exclusively, NFATp , and Western blot analysis shows that this has the same electrophoretic mobility (approximately 120 kD) as that of T lymphocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7156 10.7728 1.0000 NK cells do not express NFATc constitutively, but RNANFATc mRNA accumulation is induced in these cells within 2 h of stimulation with CD16 ligands .
1.4810 10.7732 0.9963 NK cells do not express NFATc constitutively, but proteinNFATc mRNA accumulation is induced in these cells within 2 h of stimulation with CD16 ligands .
0.8972 0.9995 0.9998 cell_typeNK cells do not express NFATc constitutively, but NFATc mRNA accumulation is induced in these cells within 2 h of stimulation with CD16 ligands .
0.8244 1.0000 1.0000 NK cells do not express proteinNFATc constitutively, but NFATc mRNA accumulation is induced in these cells within 2 h of stimulation with CD16 ligands .
1.6710 10.3800 1.0000 NK cells do not express NFATc constitutively, but NFATc mRNA accumulation is induced in these cells within 2 h of stimulation with proteinCD16 ligands .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1953 20.6956 0.9935 However, supershift assays using the available mAb recognizing the T cell NFATc revealed no detectable proteinNFATc protein in nuclear and cytoplasmic extracts from CD16- or phorbol ester -stimulated cells at any time tested, up to 4 h.
2.0877 20.2264 0.9999 However, supershift assays using the available mAb recognizing the proteinT cell NFATc revealed no detectable NFATc protein in nuclear and cytoplasmic extracts from CD16- or phorbol ester -stimulated cells at any time tested, up to 4 h.
1.7488 10.9182 10.7372 However, supershift assays using the available mAb recognizing the T cell NFATc revealed no detectable NFATc protein in nuclear and cytoplasmic extracts from CD16- or cell_linephorbol ester -stimulated cells at any time tested, up to 4 h.
0.9444 0.9999 1.0000 However, supershift assays using the available mAb recognizing the T cell proteinNFATc revealed no detectable NFATc protein in nuclear and cytoplasmic extracts from CD16- or phorbol ester -stimulated cells at any time tested, up to 4 h.
0.8456 0.9998 1.0000 However, supershift assays using the available proteinmAb recognizing the T cell NFATc revealed no detectable NFATc protein in nuclear and cytoplasmic extracts from CD16- or phorbol ester -stimulated cells at any time tested, up to 4 h.
2.1687 20.2122 1.0000 However, supershift assays using the available mAb recognizing the T cell NFATc revealed no detectable proteinNFATc protein in nuclear and cytoplasmic extracts from CD16- or phorbol ester -stimulated cells at any time tested, up to 4 h.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5923 30.0956 10.3639 These results provide the first direct evidence that both proteinCsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
2.5243 20.7562 1.0000 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of RNANFATc mRNA .
2.1291 20.9439 0.9922 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of proteinNFATc mRNA .
1.6894 10.0189 1.0000 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of proteinNFATp and subsequently induced expression of NFATc mRNA .
1.6370 10.6313 0.9999 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in cell_typeNK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
1.4095 1.0000 10.0967 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human cell_typeNK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
0.9490 1.0000 1.0000 These results provide the first direct evidence that both CsA -sensitive transcription factors , proteinNFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
0.9085 1.0000 1.0000 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and proteinNFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
0.8367 0.9987 0.9999 These results provide the first direct evidence that both CsA -sensitive proteintranscription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
3.6920 20.7811 10.6788 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in cell_typehuman NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
2.1635 20.2297 0.9998 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in cell_typeprimary cells by a single stimulus, that, in the case of CD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
0.8523 1.0000 1.0000 These results provide the first direct evidence that both CsA -sensitive transcription factors , NFATp and NFATc , are expressed in human NK cells , and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of proteinCD16 in NK cells , results in early activation of NFATp and subsequently induced expression of NFATc mRNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1004 20.2721 0.9999 Interleukin 2 signaling involves the phosphorylation of proteinStat proteins .
0.9061 0.9999 1.0000 proteinInterleukin 2 signaling involves the phosphorylation of Stat proteins .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0184 10.6414 10.9782 One of the most important cytokines involved in immune response regulation is interleukin 2 (IL-2), a potent activator of the proliferation and function of T lymphocytes and cell_typenatural killer cells .
2.1564 20.1425 10.1263 One of the most important cytokines involved in immune response regulation is interleukin 2 (IL-2), a potent activator of the proliferation and function of cell_typeT lymphocytes and natural killer cells .
0.8675 0.9999 1.0000 One of the most important proteincytokines involved in immune response regulation is interleukin 2 (IL-2), a potent activator of the proliferation and function of T lymphocytes and natural killer cells .
2.2104 20.7964 0.9997 One of the most important cytokines involved in immune response regulation is proteininterleukin 2 (IL-2), a potent activator of the proliferation and function of T lymphocytes and natural killer cells .
One of the most important cytokines involved in immune response regulation is interleukin 2 (IL-2), a potent activator of the proliferation and function of T cell_typelymphocytes and natural killer cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6458 10.7521 1.0000 The mechanisms by which the effects of proteinIL-2 are propagated within cells are not understood.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7493 10.3313 1.0000 While the binding of proteinIL-2 to its receptor was recently shown to lead to the activation of two kinases , Jak-1 and Jak-3 , subsequent steps in the signaling pathway to the nucleus that lead to the activation of specific genes had not been characterized.
0.9809 1.0000 1.0000 While the binding of IL-2 to its receptor was recently shown to lead to the activation of two kinases , Jak-1 and proteinJak-3 , subsequent steps in the signaling pathway to the nucleus that lead to the activation of specific genes had not been characterized.
0.9531 1.0000 1.0000 While the binding of IL-2 to its receptor was recently shown to lead to the activation of two kinases , proteinJak-1 and Jak-3 , subsequent steps in the signaling pathway to the nucleus that lead to the activation of specific genes had not been characterized.
0.8937 1.0000 1.0000 While the binding of IL-2 to its receptor was recently shown to lead to the activation of two proteinkinases , Jak-1 and Jak-3 , subsequent steps in the signaling pathway to the nucleus that lead to the activation of specific genes had not been characterized.
0.6918 1.0000 1.0000 While the binding of IL-2 to its proteinreceptor was recently shown to lead to the activation of two kinases , Jak-1 and Jak-3 , subsequent steps in the signaling pathway to the nucleus that lead to the activation of specific genes had not been characterized.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7460 10.6086 1.0000 Since many proteincytokines that activate Jak kinases also lead to the tyrosine phosphorylation and activation of members of the Stat family of transcription factors , the ability of IL-2 to trigger Stat phosphorylation was examined.
1.6792 10.0222 1.0000 Since many cytokines that activate Jak kinases also lead to the tyrosine phosphorylation and activation of members of the Stat family of transcription factors , the ability of proteinIL-2 to trigger Stat phosphorylation was examined.
1.6326 10.6392 1.0000 Since many cytokines that activate Jak kinases also lead to the tyrosine phosphorylation and activation of members of the Stat family of proteintranscription factors , the ability of IL-2 to trigger Stat phosphorylation was examined.
1.5027 10.8844 1.0000 Since many cytokines that activate Jak kinases also lead to the tyrosine phosphorylation and activation of members of the proteinStat family of transcription factors , the ability of IL-2 to trigger Stat phosphorylation was examined.
1.5027 10.7663 1.0000 Since many cytokines that activate proteinJak kinases also lead to the tyrosine phosphorylation and activation of members of the Stat family of transcription factors , the ability of IL-2 to trigger Stat phosphorylation was examined.
0.8466 1.0000 1.0000 Since many cytokines that activate Jak kinases also lead to the tyrosine phosphorylation and activation of members of the Stat family of transcription factors , the ability of IL-2 to trigger proteinStat phosphorylation was examined.
Since many cytokines that activate Jak proteinkinases also lead to the tyrosine phosphorylation and activation of members of the Stat family of transcription factors , the ability of IL-2 to trigger Stat phosphorylation was examined.
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.3445 30.0240 10.6188 Exposure of activated human T lymphocytes or of a cell_linenatural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
1.9757 20.7547 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two proteinStat-related proteins , p94 and p95 .
1.5923 10.3906 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to proteinIL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
1.5379 10.4331 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , proteinStat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
1.5268 10.6316 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and proteinStat3 , as well as of two Stat-related proteins , p94 and p95 .
1.4148 10.8179 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of proteinStat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
0.9194 1.0000 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and proteinp95 .
0.9092 1.0000 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( cell_lineNKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
0.8875 1.0000 1.0000 Exposure of activated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , proteinp94 and p95 .
3.3725 20.9462 20.1974 Exposure of cell_typeactivated human T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
Exposure of activated human cell_typeT lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
Exposure of activated human T lymphocytes or of a cell_typenatural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
Exposure of activated cell_typehuman T lymphocytes or of a natural killer cell line ( NKL ) to IL-2 leads to the phosphorylation of Stat1 alpha , Stat1 beta , and Stat3 , as well as of two Stat-related proteins , p94 and p95 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5501 20.5786 10.4972 p94 and p95 share homology with Stat1 at the phosphorylation site and in the proteinSrc homology 2 (SH2) domain , but otherwise are immunologically distinct from Stat1 .
1.3917 10.1005 1.0000 p94 and p95 share homology with proteinStat1 at the phosphorylation site and in the Src homology 2 (SH2) domain , but otherwise are immunologically distinct from Stat1 .
1.2193 10.7454 1.0000 p94 and p95 share homology with Stat1 at the phosphorylation site and in the Src homology 2 (SH2) domain , but otherwise are immunologically distinct from proteinStat1 .
1.1741 10.5286 0.9999 p94 and p95 share homology with Stat1 at the proteinphosphorylation site and in the Src homology 2 (SH2) domain , but otherwise are immunologically distinct from Stat1 .
0.9726 1.0000 1.0000 proteinp94 and p95 share homology with Stat1 at the phosphorylation site and in the Src homology 2 (SH2) domain , but otherwise are immunologically distinct from Stat1 .
0.9362 1.0000 1.0000 p94 and proteinp95 share homology with Stat1 at the phosphorylation site and in the Src homology 2 (SH2) domain , but otherwise are immunologically distinct from Stat1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5570 10.9587 1.0000 These proteinStat proteins were found to translocate to the nucleus and to bind to a specific DNA sequence .
2.2720 20.4026 0.9999 These Stat proteins were found to translocate to the nucleus and to bind to a specific DNADNA sequence .
These Stat proteins were found to translocate to the nucleus and to bind to a DNAspecific DNA sequence .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6774 10.1904 1.0000 These findings suggest a mechanism by which proteinIL-2 binding to its receptor may activate specific genes involved in immune cell function .
1.3904 10.9604 0.9997 These findings suggest a mechanism by which IL-2 binding to its receptor may activate specific genes involved in cell_typeimmune cell function .
0.5404 0.9998 1.0000 These findings suggest a mechanism by which IL-2 binding to its receptor may activate specific DNAgenes involved in immune cell function .
These findings suggest a mechanism by which IL-2 binding to its receptor may activate DNAspecific genes involved in immune cell function .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5399 10.8713 1.0000 Expression of DNAc-fos correlates with IFN-alpha responsiveness in Philadelphia chromosome positive chronic myelogenous leukemia .
0.8690 1.0000 1.0000 Expression of c-fos correlates with proteinIFN-alpha responsiveness in Philadelphia chromosome positive chronic myelogenous leukemia .
1.4856 10.7718 1.0000 Expression of c-fos correlates with IFN-alpha responsiveness in DNAPhiladelphia chromosome positive chronic myelogenous leukemia .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4931 20.0474 1.0000 This study evaluates (i) constitutive levels of oncogene and p53 transcripts in chronic phase CML patients and (ii) their modulations subsequent to in vivo therapy with proteinrIFN-alpha 2c .
This study evaluates (i) constitutive levels of DNAoncogene and p53 transcripts in chronic phase CML patients and (ii) their modulations subsequent to in vivo therapy with rIFN-alpha 2c .
This study evaluates (i) constitutive levels of oncogene and RNAp53 transcripts in chronic phase CML patients and (ii) their modulations subsequent to in vivo therapy with rIFN-alpha 2c .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2715 20.4998 10.6374 Peripheral blood mononuclear cells ( pbmc ) and cell_typebone marrow cells of 26 patients were examined for c-fos , c-myc , p53 and the hybrid bcr/abl mRNA levels .
1.6735 0.9972 10.3488 cell_typePeripheral blood mononuclear cells ( pbmc ) and bone marrow cells of 26 patients were examined for c-fos , c-myc , p53 and the hybrid bcr/abl mRNA levels .
0.9077 0.9999 1.0000 Peripheral blood mononuclear cells ( cell_typepbmc ) and bone marrow cells of 26 patients were examined for c-fos , c-myc , p53 and the hybrid bcr/abl mRNA levels .
3.1679 20.8413 10.9338 Peripheral blood mononuclear cells ( pbmc ) and bone marrow cells of 26 patients were examined for c-fos , c-myc , p53 and the RNAhybrid bcr/abl mRNA levels .
0.6995 1.0000 1.0000 Peripheral blood mononuclear cells ( pbmc ) and bone marrow cells of 26 patients were examined for c-fos , DNAc-myc , p53 and the hybrid bcr/abl mRNA levels .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4501 20.9881 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the DNAhybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
2.4369 20.7795 0.9999 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of cell_typeimmature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
1.8167 10.0715 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to proteinIFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
1.8146 10.1556 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to proteinIFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
1.7375 10.4942 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of cell_typelymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
1.0066 10.1281 0.9997 Results indicated that (i) constitutive RNAc-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
0.8699 0.9982 0.9999 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of RNAc-myc mRNA levels in responder patients .
0.8363 1.0000 0.9999 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the cell_typepbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
1.4698 10.7811 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of proteinc-fos and downregulation of c-myc mRNA levels in responder patients .
0.9662 1.0000 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and proteinp53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
0.8009 1.0000 1.0000 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , proteinc-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
0.7840 0.9999 0.9993 Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive RNAmRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) RNAconstitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of DNAc-fos and downregulation of c-myc mRNA levels in responder patients .
Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , c-myc and DNAp53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
Results indicated that (i) constitutive c-fos transcript levels are significantly higher in patients subsequently responding to IFN-alpha therapy (p < 0.01) and positively correlated with the proportion of lymphocytes (r = 0.6895, p < 0.01) and negatively with the proportion of immature cells (r = -0.568, p < 0.01) contained in the pbmc preparations tested, (ii) constitutive mRNA levels of the hybrid bcr/abl , DNAc-myc and p53 are positively correlated with each other, but failed to relate to disease parameters, and (iii) acute and chronic in vivo exposure to IFN-alpha is accompanied by upregulation of c-fos and downregulation of c-myc mRNA levels in responder patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0363 20.4575 10.4843 Menopause is associated with a significant increase in blood monocyte number and a relative decrease in the expression of estrogen receptors in cell_typehuman peripheral monocytes .
2.1837 20.7536 0.9999 Menopause is associated with a significant increase in blood monocyte number and a relative decrease in the expression of proteinestrogen receptors in human peripheral monocytes .
2.2578 20.1298 0.9999 Menopause is associated with a significant increase in cell_typeblood monocyte number and a relative decrease in the expression of estrogen receptors in human peripheral monocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2070 20.7427 1.0000 PROBLEM: The clinical significance of the differential expression of proteinestrogen receptor ( ER ) in human monocytes was evaluated.
1.5096 10.5289 0.9999 PROBLEM: The clinical significance of the differential expression of estrogen receptor ( ER ) in cell_typehuman monocytes was evaluated.
0.9697 1.0000 1.0000 PROBLEM: The clinical significance of the differential expression of estrogen receptor ( proteinER ) in human monocytes was evaluated.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9368 0.9999 1.0000 In addition, the monocyte and cell_typelymphocyte counts and the blood estrogen levels of each patient were determine.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0436 20.5767 10.8115 RESULTS: During menopause there is a significant decrease in the percentage of cell_typeER positive monocytes , and an increase in blood monocyte number , which declines following estrogen replacement therapy to values of the young.
2.3522 20.2909 0.9944 RESULTS: During menopause there is a significant decrease in the percentage of proteinER positive monocytes , and an increase in blood monocyte number , which declines following estrogen replacement therapy to values of the young.
0.9099 1.0000 1.0000 RESULTS: During menopause there is a significant decrease in the percentage of ER positive monocytes , and an increase in blood cell_typemonocyte number , which declines following estrogen replacement therapy to values of the young.
0.9591 1.0000 1.0000 RESULTS: During menopause there is a significant decrease in the percentage of ER positive cell_typemonocytes , and an increase in blood monocyte number , which declines following estrogen replacement therapy to values of the young.
RESULTS: During menopause there is a significant decrease in the percentage of ER positive monocytes , and an increase in cell_typeblood monocyte number , which declines following estrogen replacement therapy to values of the young.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7662 10.6680 1.0000 CONCLUSIONS: These findings suggest that estrogen modulates the monocyte numbers and its effects may be mediated through the proteinER in the monocytes .
1.7592 10.4221 1.0000 CONCLUSIONS: These findings suggest that estrogen modulates the monocyte numbers and its effects may be mediated through the ER in the cell_typemonocytes .
0.8085 1.0000 1.0000 CONCLUSIONS: These findings suggest that estrogen modulates the cell_typemonocyte numbers and its effects may be mediated through the ER in the monocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1782 20.6003 20.9399 Staphylococcal enterotoxins modulate interleukin 2 receptor expression and ligand-induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and proteinsignal transducers and activators of transcription ( Stat proteins ).
4.9497 30.8607 20.4804 Staphylococcal enterotoxins modulate interleukin 2 receptor expression and ligand-induced tyrosine phosphorylation of the proteinJanus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription ( Stat proteins ).
2.6119 30.2762 10.0721 Staphylococcal enterotoxins modulate proteininterleukin 2 receptor expression and ligand-induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription ( Stat proteins ).
1.5352 10.3257 0.9999 Staphylococcal enterotoxins modulate interleukin 2 receptor expression and ligand-induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription ( proteinStat proteins ).
0.9519 1.0000 1.0000 Staphylococcal enterotoxins modulate interleukin 2 receptor expression and ligand-induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( proteinJak3 ) and signal transducers and activators of transcription ( Stat proteins ).
proteinStaphylococcal enterotoxins modulate interleukin 2 receptor expression and ligand-induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription ( Stat proteins ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7163 20.8270 10.7877 Staphylococcal enterotoxins ( SE ) stimulate T cells expressing the appropriate proteinvariable region beta chain of ( V beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
1.4735 10.6485 0.9998 Staphylococcal enterotoxins ( SE ) stimulate cell_typeT cells expressing the appropriate variable region beta chain of ( V beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
0.9298 1.0000 1.0000 Staphylococcal enterotoxins ( proteinSE ) stimulate T cells expressing the appropriate variable region beta chain of ( V beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
0.7028 0.9972 0.9999 proteinStaphylococcal enterotoxins ( SE ) stimulate T cells expressing the appropriate variable region beta chain of ( V beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
4.7973 20.1031 20.4115 Staphylococcal enterotoxins ( SE ) stimulate T cells expressing the appropriate variable region beta chain of protein( V beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
1.5070 0.9998 10.9399 Staphylococcal enterotoxins ( SE ) stimulate T cells expressing the appropriate variable region beta chain of ( proteinV beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
Staphylococcal enterotoxins ( SE ) stimulate T cells expressing the appropriate variable region beta chain of ( proteinV beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
Staphylococcal enterotoxins ( SE ) stimulate T cells expressing the appropriate proteinvariable region beta chain of ( V beta ) T-cell receptors and have been implicated in the pathogenesis of several autoimmune diseases .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3074 20.3903 0.9998 Depending on costimulatory signals , SE induce either proliferation or anergy in cell_typeT cells .
1.0448 10.0052 1.0000 Depending on costimulatory signals , proteinSE induce either proliferation or anergy in T cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9833 1.0000 1.0000 In addition, SE can induce an interleukin-2 ( proteinIL-2 ) nonresponsive state and apoptosis .
0.8437 1.0000 0.9999 In addition, SE can induce an proteininterleukin-2 ( IL-2 ) nonresponsive state and apoptosis .
In addition, proteinSE can induce an interleukin-2 ( IL-2 ) nonresponsive state and apoptosis .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8611 20.5893 10.8196 Here, we show that SE induce dynamic changes in the expression of and signal transduction through the IL-2 receptor (IL-2R) beta and gamma chains ( IL-2R beta and IL-2R gamma ) in cell_linehuman antigen-specific CD4+ T-cell lines .
1.6128 10.3746 1.0000 Here, we show that SE induce dynamic changes in the expression of and signal transduction through the IL-2 receptor (IL-2R) beta and gamma chains ( IL-2R beta and proteinIL-2R gamma ) in human antigen-specific CD4+ T-cell lines .
0.8198 0.9997 1.0000 Here, we show that SE induce dynamic changes in the expression of and signal transduction through the IL-2 receptor (IL-2R) beta and gamma chains ( proteinIL-2R beta and IL-2R gamma ) in human antigen-specific CD4+ T-cell lines .
0.7890 1.0000 0.9933 Here, we show that SE induce dynamic changes in the expression of and signal transduction through the proteinIL-2 receptor (IL-2R) beta and gamma chains ( IL-2R beta and IL-2R gamma ) in human antigen-specific CD4+ T-cell lines .
Here, we show that proteinSE induce dynamic changes in the expression of and signal transduction through the IL-2 receptor (IL-2R) beta and gamma chains ( IL-2R beta and IL-2R gamma ) in human antigen-specific CD4+ T-cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3683 20.2203 0.9999 Thus, after 4 hr of exposure to SEA and SEB , the expression of IL-2R beta was down-regulated, IL-2R gamma was slightly up-regulated, while proteinIL-2R alpha remained largely unaffected.
2.3365 20.3607 1.0000 Thus, after 4 hr of exposure to SEA and SEB , the expression of proteinIL-2R beta was down-regulated, IL-2R gamma was slightly up-regulated, while IL-2R alpha remained largely unaffected.
1.6895 10.8786 1.0000 Thus, after 4 hr of exposure to SEA and SEB , the expression of IL-2R beta was down-regulated, proteinIL-2R gamma was slightly up-regulated, while IL-2R alpha remained largely unaffected.
1.6668 10.3296 1.0000 Thus, after 4 hr of exposure to proteinSEA and SEB , the expression of IL-2R beta was down-regulated, IL-2R gamma was slightly up-regulated, while IL-2R alpha remained largely unaffected.
0.9430 1.0000 1.0000 Thus, after 4 hr of exposure to SEA and proteinSEB , the expression of IL-2R beta was down-regulated, IL-2R gamma was slightly up-regulated, while IL-2R alpha remained largely unaffected.
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.1453 30.7123 20.2114 The changes in the composition of IL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the proteinJanus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription called Stat3 and Stat5 .
1.4109 10.7917 1.0000 The changes in the composition of proteinIL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription called Stat3 and Stat5 .
0.9689 1.0000 1.0000 The changes in the composition of IL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( proteinJak3 ) and signal transducers and activators of transcription called Stat3 and Stat5 .
0.9388 1.0000 1.0000 The changes in the composition of IL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription called proteinStat3 and Stat5 .
0.9376 1.0000 1.0000 The changes in the composition of IL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription called Stat3 and proteinStat5 .
0.9082 1.0000 1.0000 The changes in the composition of IL-2Rs were accompanied by inhibition of proteinIL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and activators of transcription called Stat3 and Stat5 .
2.8950 10.7892 10.9025 The changes in the composition of IL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and signal transducers and proteinactivators of transcription called Stat3 and Stat5 .
The changes in the composition of IL-2Rs were accompanied by inhibition of IL-2 -induced tyrosine phosphorylation of the Janus protein- tyrosine kinase 3 ( Jak3 ) and proteinsignal transducers and activators of transcription called Stat3 and Stat5 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7171 10.2240 1.0000 In parallel experiments, proteinIL-2 -driven proliferation was inhibited significantly.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7311 10.7642 1.0000 After 16 hr of exposure to SE , the expression of IL-2R beta remained low, while that of IL2R alpha and proteinIL2R gamma was further up-regulated, and ligand-induced tyrosine phosphorylation of Jak3 and Stat proteins was partly normalized.
1.6688 10.8717 1.0000 After 16 hr of exposure to SE , the expression of IL-2R beta remained low, while that of IL2R alpha and IL2R gamma was further up-regulated, and ligand-induced tyrosine phosphorylation of proteinJak3 and Stat proteins was partly normalized.
1.6387 10.9465 1.0000 After 16 hr of exposure to SE , the expression of proteinIL-2R beta remained low, while that of IL2R alpha and IL2R gamma was further up-regulated, and ligand-induced tyrosine phosphorylation of Jak3 and Stat proteins was partly normalized.
1.6347 10.7239 1.0000 After 16 hr of exposure to SE , the expression of IL-2R beta remained low, while that of proteinIL2R alpha and IL2R gamma was further up-regulated, and ligand-induced tyrosine phosphorylation of Jak3 and Stat proteins was partly normalized.
1.6243 10.5600 1.0000 After 16 hr of exposure to SE , the expression of IL-2R beta remained low, while that of IL2R alpha and IL2R gamma was further up-regulated, and ligand-induced tyrosine phosphorylation of Jak3 and proteinStat proteins was partly normalized.
After 16 hr of exposure to proteinSE , the expression of IL-2R beta remained low, while that of IL2R alpha and IL2R gamma was further up-regulated, and ligand-induced tyrosine phosphorylation of Jak3 and Stat proteins was partly normalized.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4596 10.8947 0.9999 Yet, IL-2 -driven proliferation remained profoundly inhibited, suggesting that signaling events other than proteinJak3 /Stat activation had also been changed following SE stimulation .
0.9691 1.0000 1.0000 Yet, IL-2 -driven proliferation remained profoundly inhibited, suggesting that signaling events other than Jak3 protein/Stat activation had also been changed following SE stimulation .
0.9444 1.0000 1.0000 Yet, proteinIL-2 -driven proliferation remained profoundly inhibited, suggesting that signaling events other than Jak3 /Stat activation had also been changed following SE stimulation .
Yet, IL-2 -driven proliferation remained profoundly inhibited, suggesting that signaling events other than Jak3 /Stat activation had also been changed following proteinSE stimulation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8419 20.2280 10.9325 In conclusion, our data suggest that SE can modulate IL-2R expression and signal transduction involving the Jak/Stat pathway in cell_lineCD4+ T-cell lines .
1.5753 10.3272 1.0000 In conclusion, our data suggest that SE can modulate proteinIL-2R expression and signal transduction involving the Jak/Stat pathway in CD4+ T-cell lines .
0.9345 1.0000 1.0000 In conclusion, our data suggest that SE can modulate IL-2R expression and signal transduction involving the proteinJak/Stat pathway in CD4+ T-cell lines .
In conclusion, our data suggest that proteinSE can modulate IL-2R expression and signal transduction involving the Jak/Stat pathway in CD4+ T-cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8738 20.7564 10.9218 Constitutive NF-kappa B activation , enhanced granulopoiesis , and neonatal lethality in proteinI kappa B alpha -deficient mice .
1.5386 10.5915 1.0000 Constitutive proteinNF-kappa B activation , enhanced granulopoiesis , and neonatal lethality in I kappa B alpha -deficient mice .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3136 20.5294 10.7640 Transcription factors belonging to the NF-kappa B family are controlled by inhibitory I kappa B proteins , mainly proteinI kappa B alpha and I kappa B beta .
3.8054 20.9690 10.8749 Transcription factors belonging to the NF-kappa B family are controlled by inhibitory I kappa B proteins , mainly I kappa B alpha and proteinI kappa B beta .
2.1015 20.5239 0.9999 Transcription factors belonging to the proteinNF-kappa B family are controlled by inhibitory I kappa B proteins , mainly I kappa B alpha and I kappa B beta .
1.4104 20.5931 0.7224 Transcription factors belonging to the proteinNF-kappa B family are controlled by inhibitory I kappa B proteins , mainly I kappa B alpha and I kappa B beta .
0.8398 0.9995 1.0000 proteinTranscription factors belonging to the NF-kappa B family are controlled by inhibitory I kappa B proteins , mainly I kappa B alpha and I kappa B beta .
4.3887 20.3073 10.6697 Transcription factors belonging to the NF-kappa B family are controlled by inhibitory proteinI kappa B proteins , mainly I kappa B alpha and I kappa B beta .
Transcription factors belonging to the NF-kappa B family are controlled by proteininhibitory I kappa B proteins , mainly I kappa B alpha and I kappa B beta .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.0493 20.9403 10.8192 Apparently normal at birth, proteinI kappa B alpha -/- mice exhibit severe runting, skin defects , and extensive granulopoiesis postnatally, typically dying by 8 days.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8901 20.3707 10.2257 Hematopoietic tissues from these mice display elevated levels of both proteinnuclear NF-kappa B and mRNAs of some, but not all, genes thought to be regulated by NF-kappa B .
2.2953 20.2071 0.9999 Hematopoietic tissues from these mice display elevated levels of both nuclear NF-kappa B and mRNAs of some, but not all, genes thought to be regulated by proteinNF-kappa B .
0.9377 0.9999 1.0000 Hematopoietic tissues from these mice display elevated levels of both nuclear NF-kappa B and RNAmRNAs of some, but not all, genes thought to be regulated by NF-kappa B .
0.7616 0.9999 0.9999 Hematopoietic tissues from these mice display elevated levels of both nuclear proteinNF-kappa B and mRNAs of some, but not all, genes thought to be regulated by NF-kappa B .
0.5230 0.9987 0.9999 cell_typeHematopoietic tissues from these mice display elevated levels of both nuclear NF-kappa B and mRNAs of some, but not all, genes thought to be regulated by NF-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6665 20.9467 10.5692 NF-kappa B elevation results in these phenotypic abnormalities because mice lacking both proteinI kappa B alpha and the p50 subunit of NF-kappa B show a dramatically delayed onset of abnormalities .
2.0276 20.2645 1.0000 NF-kappa B elevation results in these phenotypic abnormalities because mice lacking both I kappa B alpha and the proteinp50 subunit of NF-kappa B show a dramatically delayed onset of abnormalities .
1.5947 10.9896 0.9999 NF-kappa B elevation results in these phenotypic abnormalities because mice lacking both I kappa B alpha and the p50 subunit of proteinNF-kappa B show a dramatically delayed onset of abnormalities .
0.9014 1.0000 1.0000 proteinNF-kappa B elevation results in these phenotypic abnormalities because mice lacking both I kappa B alpha and the p50 subunit of NF-kappa B show a dramatically delayed onset of abnormalities .
1.6953 20.6325 0.9874 NF-kappa B elevation results in these phenotypic abnormalities because mice lacking both I kappa B alpha and the proteinp50 subunit of NF-kappa B show a dramatically delayed onset of abnormalities .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3062 20.6908 10.8166 In contrast to hematopoietic cells , I kappa B alpha -/- embryonic fibroblasts show minimal constitutive NF-kappa B , as well as normal signal-dependent NF-kappa B activation that is concomitant with proteinI kappa B beta degradation .
4.0919 20.9559 10.6987 In contrast to hematopoietic cells , cell_lineI kappa B alpha -/- embryonic fibroblasts show minimal constitutive NF-kappa B , as well as normal signal-dependent NF-kappa B activation that is concomitant with I kappa B beta degradation .
2.9005 10.8926 10.8703 In contrast to hematopoietic cells , proteinI kappa B alpha -/- embryonic fibroblasts show minimal constitutive NF-kappa B , as well as normal signal-dependent NF-kappa B activation that is concomitant with I kappa B beta degradation .
2.5350 20.6669 10.0491 In contrast to cell_typehematopoietic cells , I kappa B alpha -/- embryonic fibroblasts show minimal constitutive NF-kappa B , as well as normal signal-dependent NF-kappa B activation that is concomitant with I kappa B beta degradation .
1.3798 10.5288 1.0000 In contrast to hematopoietic cells , I kappa B alpha -/- embryonic fibroblasts show minimal constitutive NF-kappa B , as well as normal signal-dependent proteinNF-kappa B activation that is concomitant with I kappa B beta degradation .
1.2930 10.7157 0.9999 In contrast to hematopoietic cells , I kappa B alpha -/- embryonic fibroblasts show minimal constitutive proteinNF-kappa B , as well as normal signal-dependent NF-kappa B activation that is concomitant with I kappa B beta degradation .
In contrast to hematopoietic cells , I kappa B alpha -/- embryonic fibroblasts show minimal proteinconstitutive NF-kappa B , as well as normal signal-dependent NF-kappa B activation that is concomitant with I kappa B beta degradation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1733 30.9660 10.8104 Our results indicate that I kappa b beta, but not proteinI kappa B alpha , is required for the signal-dependent activation of NF-kappa B in fibroblasts .
1.9480 20.8132 0.9999 Our results indicate that I kappa b beta, but not I kappa B alpha , is required for the signal-dependent activation of proteinNF-kappa B in fibroblasts .
1.5443 10.5112 0.9998 Our results indicate that I kappa b beta, but not I kappa B alpha , is required for the signal-dependent activation of NF-kappa B in cell_typefibroblasts .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3026 10.8582 10.1837 However, proteinI kappa B alpha is required for the postinduction repression of NF-kappa B in fibroblasts .
1.9825 20.5339 0.9999 However, I kappa B alpha is required for the postinduction repression of proteinNF-kappa B in fibroblasts .
1.5127 10.4329 0.9999 However, I kappa B alpha is required for the postinduction repression of NF-kappa B in cell_typefibroblasts .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6808 20.7285 10.5536 These results define distinct roles for the two forms of proteinI kappa B and demonstrate the necessity for stringent control of NF-kappa B .
2.1827 20.5561 1.0000 These results define distinct roles for the two forms of I kappa B and demonstrate the necessity for stringent control of proteinNF-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9770 1.0000 1.0000 proteinInterleukin-7 can induce the activation of Jak 1 , Jak 3 and STAT 5 proteins in murine T cells .
3.5375 20.9010 10.9154 Interleukin-7 can induce the activation of Jak 1 , Jak 3 and STAT 5 proteins in cell_typemurine T cells .
Interleukin-7 can induce the activation of proteinJak 1 , Jak 3 and STAT 5 proteins in murine T cells .
Interleukin-7 can induce the activation of Jak 1 , proteinJak 3 and STAT 5 proteins in murine T cells .
Interleukin-7 can induce the activation of Jak 1 , Jak 3 and proteinSTAT 5 proteins in murine T cells .
Interleukin-7 can induce the activation of Jak 1 , Jak 3 and STAT 5 proteins in murine cell_typeT cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8541 20.4483 10.3742 The activation of Janus protein tyrosine kinases ( Jak ) and proteinSTAT ( signal transducer and activator of transcription ) proteins has recently been linked to the signal transduction mechanism of several cytokines .
2.7479 30.4411 10.1643 The activation of proteinJanus protein tyrosine kinases ( Jak ) and STAT ( signal transducer and activator of transcription ) proteins has recently been linked to the signal transduction mechanism of several cytokines .
0.9161 0.9999 1.0000 The activation of Janus protein tyrosine kinases ( proteinJak ) and STAT ( signal transducer and activator of transcription ) proteins has recently been linked to the signal transduction mechanism of several cytokines .
0.7893 0.9999 1.0000 The activation of Janus protein tyrosine kinases ( Jak ) and STAT ( signal transducer and activator of transcription ) proteins has recently been linked to the signal transduction mechanism of several proteincytokines .
0.5017 1.0000 0.9960 The activation of Janus protein tyrosine kinases ( Jak ) and proteinSTAT ( signal transducer and activator of transcription ) proteins has recently been linked to the signal transduction mechanism of several cytokines .
The activation of Janus protein tyrosine kinases ( Jak ) and STAT ( proteinsignal transducer and activator of transcription ) proteins has recently been linked to the signal transduction mechanism of several cytokines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1817 20.2337 1.0000 IL-7 was observed to induce a rapid and dose-dependent tyrosine phosphorylation of proteinJak 1 and Jak 3 and concomitantly, the tyrosine phosphorylation and DNA binding activity of multiple STAT proteins .
1.5105 10.9023 0.9999 IL-7 was observed to induce a rapid and dose-dependent tyrosine phosphorylation of Jak 1 and proteinJak 3 and concomitantly, the tyrosine phosphorylation and DNA binding activity of multiple STAT proteins .
0.9683 1.0000 1.0000 proteinIL-7 was observed to induce a rapid and dose-dependent tyrosine phosphorylation of Jak 1 and Jak 3 and concomitantly, the tyrosine phosphorylation and DNA binding activity of multiple STAT proteins .
0.7163 0.9999 0.9998 IL-7 was observed to induce a rapid and dose-dependent tyrosine phosphorylation of Jak 1 and Jak 3 and concomitantly, the tyrosine phosphorylation and DNA binding activity of multiple proteinSTAT proteins .
3.8024 20.6461 10.6562 IL-7 was observed to induce a rapid and dose-dependent tyrosine phosphorylation of Jak 1 and Jak 3 and concomitantly, the tyrosine phosphorylation and DNA binding activity of proteinmultiple STAT proteins .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8698 20.7730 10.6754 The STAT proteins utilized by IL-7 were identical to those induced by IL-2 and could be identified as various proteinSTAT 5 isoforms .
1.4987 10.8715 1.0000 The STAT proteins utilized by proteinIL-7 were identical to those induced by IL-2 and could be identified as various STAT 5 isoforms .
1.4605 10.6018 1.0000 The STAT proteins utilized by IL-7 were identical to those induced by proteinIL-2 and could be identified as various STAT 5 isoforms .
1.4423 10.8368 1.0000 The proteinSTAT proteins utilized by IL-7 were identical to those induced by IL-2 and could be identified as various STAT 5 isoforms .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8137 10.2053 1.0000 Moreover, the induction of both Jak 1 and 3 , and STAT 5 activity strongly correlated with the growth-promoting effects of IL-7 , suggesting that this signal transduction mechanism may play a key role in proteinIL-7 -induced proliferation .
1.7645 10.3036 1.0000 Moreover, the induction of both Jak 1 and 3 , and STAT 5 activity strongly correlated with the growth-promoting effects of proteinIL-7 , suggesting that this signal transduction mechanism may play a key role in IL-7 -induced proliferation .
1.6907 10.8470 1.0000 Moreover, the induction of both Jak 1 and 3 , and proteinSTAT 5 activity strongly correlated with the growth-promoting effects of IL-7 , suggesting that this signal transduction mechanism may play a key role in IL-7 -induced proliferation .
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0.9838 1.0000 1.0000 proteinCytokine -modulating activity of tepoxalin , a new potential antirheumatic .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9126 1.0000 1.0000 Tepoxalin is a new dual proteincyclooxygenase/5-lipoxygenase anti-inflammatory compound currently under clinical investigation.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7871 10.2958 1.0000 It has been shown to possess anti-inflammatory activity in a variety of animal models and more recently to inhibit proteinIL-2 induced signal transduction .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9435 1.0000 1.0000 The current study was conducted to evaluate the proteincytokine modulating activity of tepoxalin and the role of iron in these effects.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1022 10.7704 20.7681 In cell_typehuman peripheral blood mononuclear cells ( PBMC ) stimulated with OKT3/PMA , tepoxalin inhibited lymphocyte proliferation with an IC50 of 6 microM.
0.9208 1.0000 1.0000 In human peripheral blood mononuclear cells ( cell_typePBMC ) stimulated with OKT3/PMA , tepoxalin inhibited lymphocyte proliferation with an IC50 of 6 microM.
0.5240 0.9997 1.0000 In human peripheral blood mononuclear cells ( PBMC ) stimulated with proteinOKT3/PMA , tepoxalin inhibited lymphocyte proliferation with an IC50 of 6 microM.
In human peripheral blood mononuclear cells ( PBMC ) stimulated with OKT3/PMA , tepoxalin inhibited cell_typelymphocyte proliferation with an IC50 of 6 microM.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6220 10.6248 1.0000 Additionally, it inhibited the production of LTB4 (IC50 = 0.5 microM) and the proteincytokines IL-2 , IL-6 and TNF alpha (IC50 = 10-12 microM).
0.9786 1.0000 1.0000 Additionally, it inhibited the production of LTB4 (IC50 = 0.5 microM) and the cytokines IL-2 , proteinIL-6 and TNF alpha (IC50 = 10-12 microM).
0.9559 1.0000 1.0000 Additionally, it inhibited the production of LTB4 (IC50 = 0.5 microM) and the cytokines proteinIL-2 , IL-6 and TNF alpha (IC50 = 10-12 microM).
0.8320 0.9998 1.0000 Additionally, it inhibited the production of LTB4 (IC50 = 0.5 microM) and the cytokines IL-2 , IL-6 and proteinTNF alpha (IC50 = 10-12 microM).
Additionally, it inhibited the production of proteinLTB4 (IC50 = 0.5 microM) and the cytokines IL-2 , IL-6 and TNF alpha (IC50 = 10-12 microM).
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6536 10.7604 1.0000 Add-back experiments with either proteincytokines ( IL-2 or IL-6 ), LTB4 or conditioned media failed to restore the proliferative response in the presence of tepoxalin .
0.9633 1.0000 1.0000 Add-back experiments with either cytokines ( IL-2 or proteinIL-6 ), LTB4 or conditioned media failed to restore the proliferative response in the presence of tepoxalin .
0.9316 1.0000 1.0000 Add-back experiments with either cytokines ( proteinIL-2 or IL-6 ), LTB4 or conditioned media failed to restore the proliferative response in the presence of tepoxalin .
Add-back experiments with either cytokines ( IL-2 or IL-6 ), proteinLTB4 or conditioned media failed to restore the proliferative response in the presence of tepoxalin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5888 20.6696 10.4157 Tepoxalin also inhibits the activation of proteinNF kappa B , a transcription factor which acts on several cytokine genes .
2.1184 20.7838 0.9998 Tepoxalin also inhibits the activation of NF kappa B , a transcription factor which acts on several DNAcytokine genes .
2.0522 20.1083 0.9999 Tepoxalin also inhibits the activation of NF kappa B , a proteintranscription factor which acts on several cytokine genes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7280 20.7782 10.4479 Tepoxalin 's effect on proteinNF kappa B is also reversed by the addition of iron salts .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0434 20.5083 10.2557 These data suggest that the action of tepoxalin to inhibit proliferation in PBMC may be at least in part due to its ability to reduce the amount of available iron resulting in decreased activation of proteinNF kappa B and subsequent inhibition of cytokine production .
1.6961 10.7895 1.0000 These data suggest that the action of tepoxalin to inhibit proliferation in cell_typePBMC may be at least in part due to its ability to reduce the amount of available iron resulting in decreased activation of NF kappa B and subsequent inhibition of cytokine production .
0.8942 1.0000 1.0000 These data suggest that the action of tepoxalin to inhibit proliferation in PBMC may be at least in part due to its ability to reduce the amount of available iron resulting in decreased activation of NF kappa B and subsequent inhibition of proteincytokine production .
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4.2914 20.9623 20.5715 N- and C-terminal sequences control degradation of proteinMAD3/ I kappa B alpha in response to inducers of NF-kappa B activity .
2.1417 20.7427 1.0000 N- and C-terminal sequences control degradation of MAD3/ I kappa B alpha in response to inducers of proteinNF-kappa B activity .
1.3060 0.9998 10.9548 N- and C-terminal sequences control degradation of MAD3/ proteinI kappa B alpha in response to inducers of NF-kappa B activity .
proteinN- and C-terminal sequences control degradation of MAD3/ I kappa B alpha in response to inducers of NF-kappa B activity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0014 20.4191 0.9995 The proteolytic degradation of the inhibitory protein MAD3/ I kappa B alpha in response to extracellular stimulation is a prerequisite step in the activation of the proteintranscription factor NF-kappa B .
1.9950 20.3994 0.9991 The proteolytic degradation of the proteininhibitory protein MAD3/ I kappa B alpha in response to extracellular stimulation is a prerequisite step in the activation of the transcription factor NF-kappa B .
1.6802 0.8434 10.2748 The proteolytic degradation of the inhibitory protein proteinMAD3/ I kappa B alpha in response to extracellular stimulation is a prerequisite step in the activation of the transcription factor NF-kappa B .
1.3935 0.9998 10.7389 The proteolytic degradation of the inhibitory protein MAD3/ proteinI kappa B alpha in response to extracellular stimulation is a prerequisite step in the activation of the transcription factor NF-kappa B .
0.8741 0.9989 0.9997 The proteolytic degradation of the inhibitory protein MAD3/ I kappa B alpha in response to extracellular stimulation is a prerequisite step in the activation of the transcription factor proteinNF-kappa B .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1970 30.9829 20.5808 Analysis of the expression of proteinhuman I kappa B alpha protein in stable transfectants of mouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous I kappa B alpha is degraded in response to inducers of NF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
3.8131 20.2356 10.8306 Analysis of the expression of human I kappa B alpha protein in stable transfectants of mouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous proteinI kappa B alpha is degraded in response to inducers of NF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
2.9255 10.5340 10.9191 Analysis of the expression of human I kappa B alpha protein in stable transfectants of cell_linemouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous I kappa B alpha is degraded in response to inducers of NF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
1.9989 20.5708 0.9999 Analysis of the expression of human I kappa B alpha protein in stable transfectants of mouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous I kappa B alpha is degraded in response to inducers of proteinNF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
0.6024 1.0000 0.6402 Analysis of the expression of human proteinI kappa B alpha protein in stable transfectants of mouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous I kappa B alpha is degraded in response to inducers of NF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
1.4935 30.9601 10.6238 Analysis of the expression of proteinhuman I kappa B alpha protein in stable transfectants of mouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous I kappa B alpha is degraded in response to inducers of NF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
1.4288 10.4746 0.9996 Analysis of the expression of human I kappa B alpha protein in cell_linestable transfectants of mouse 70Z/3 cells shows that, as for the endogenous murine protein, exogenous I kappa B alpha is degraded in response to inducers of NF-kappa B activity , such as phorbol myristate acetate or lipopolysaccharide .
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.5155 30.9878 20.2158 In addition, pretreatment of the cells with the proteasome inhibitor N-Ac-Leu-Leu-norleucinal inhibits this ligand-induced degradation and, in agreement with previous studies, stabilizes a hyperphosphorylated form of the proteinhuman I kappa B alpha protein .
0.8142 1.0000 1.0000 In addition, pretreatment of the cells with the proteinproteasome inhibitor N-Ac-Leu-Leu-norleucinal inhibits this ligand-induced degradation and, in agreement with previous studies, stabilizes a hyperphosphorylated form of the human I kappa B alpha protein .
0.6560 1.0000 0.5441 In addition, pretreatment of the cells with the proteasome inhibitor N-Ac-Leu-Leu-norleucinal inhibits this ligand-induced degradation and, in agreement with previous studies, stabilizes a hyperphosphorylated form of the human proteinI kappa B alpha protein .
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3.1893 30.3899 0.9998 By expressing mutant forms of the human protein in this cell line , we have been able to delineate the sequences responsible for both the ligand-induced phosphorylation and the degradation of proteinI kappa B alpha .
2.2775 20.0646 0.9999 By expressing mutant forms of the human protein in this cell_linecell line , we have been able to delineate the sequences responsible for both the ligand-induced phosphorylation and the degradation of I kappa B alpha .
2.2367 20.2490 1.0000 By expressing mutant forms of the proteinhuman protein in this cell line , we have been able to delineate the sequences responsible for both the ligand-induced phosphorylation and the degradation of I kappa B alpha .
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3.4521 20.2148 10.9325 Our results show that deletion of the C terminus of the I kappa B alpha molecule up to proteinamino acid 279 abolishes constitutive but not ligand-inducible phosphorylation and inhibits ligand-inducible degradation .
2.4159 20.2680 10.8963 Our results show that deletion of the C terminus of the proteinI kappa B alpha molecule up to amino acid 279 abolishes constitutive but not ligand-inducible phosphorylation and inhibits ligand-inducible degradation .
1.3114 10.8500 0.9999 Our results show that deletion of the proteinC terminus of the I kappa B alpha molecule up to amino acid 279 abolishes constitutive but not ligand-inducible phosphorylation and inhibits ligand-inducible degradation .
3.9193 20.2093 10.0654 Our results show that deletion of the C terminus of the proteinI kappa B alpha molecule up to amino acid 279 abolishes constitutive but not ligand-inducible phosphorylation and inhibits ligand-inducible degradation .
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4.1751 20.4183 10.7386 Further analysis reveals that the inducible phosphorylation of proteinI kappa B alpha maps to two serines in the N terminus of the protein (residues 32 and 36) and that the mutation of either residue is sufficient to abolish ligand-induced degradation, whereas both residues must be mutated to abolish inducible phosphorylation of the protein.
1.5955 10.9424 1.0000 Further analysis reveals that the inducible phosphorylation of I kappa B alpha maps to two serines in the proteinN terminus of the protein (residues 32 and 36) and that the mutation of either residue is sufficient to abolish ligand-induced degradation, whereas both residues must be mutated to abolish inducible phosphorylation of the protein.
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0.8426 1.0000 1.0000 proteinMicrotubules mediate cellular 25-hydroxyvitamin D3 trafficking and the genomic response to 1,25-dihydroxyvitamin D3 in normal human monocytes .
3.6056 20.6897 10.7594 Microtubules mediate cellular 25-hydroxyvitamin D3 trafficking and the genomic response to 1,25-dihydroxyvitamin D3 in cell_typenormal human monocytes .
Microtubules mediate cellular 25-hydroxyvitamin D3 trafficking and the genomic response to 1,25-dihydroxyvitamin D3 in normal cell_typehuman monocytes .
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1.3065 0.9999 10.7024 The genomic actions of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are mediated by the intracellular proteinvitamin D receptor ( VDR ).
0.9621 1.0000 1.0000 The genomic actions of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are mediated by the intracellular vitamin D receptor ( proteinVDR ).
3.7116 20.4407 10.9068 The genomic actions of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are mediated by the proteinintracellular vitamin D receptor ( VDR ).
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2.4847 20.8683 0.9999 Although immunocytochemistry has shown that disruption of microtubular assembly prevents nuclear access of the proteinsterol- VDR complex , the role of microtubules in the response to 1,25(OH)2D3 has not been studied in viable cells .
2.3944 20.3647 0.9998 Although immunocytochemistry has shown that disruption of microtubular assembly prevents nuclear access of the sterol- VDR complex , the role of microtubules in the response to 1,25(OH)2D3 has not been studied in cell_typeviable cells .
1.6942 10.5614 1.0000 Although immunocytochemistry has shown that disruption of microtubular assembly prevents nuclear access of the sterol- VDR complex , the role of proteinmicrotubules in the response to 1,25(OH)2D3 has not been studied in viable cells .
0.9467 1.0000 0.9873 Although immunocytochemistry has shown that disruption of microtubular assembly prevents nuclear access of the sterol- proteinVDR complex , the role of microtubules in the response to 1,25(OH)2D3 has not been studied in viable cells .
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3.4777 20.0822 10.6925 Our studies examined this interaction in cell_typenormal human monocytes .
Our studies examined this interaction in normal cell_typehuman monocytes .
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0.9096 1.0000 1.0000 cell_typeMonocytes convert 25(OH)D3 to 1,25(OH)2D3 and to 24-hydroxylated metabolites more polar than 1,25(OH)2D3 .
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1.7109 10.9237 1.0000 Microtubule disruption totally abolished the ability of exogenous 1,25(OH)2D3 to suppress its own synthesis and to induce RNA24-hydroxylase mRNA and activity, without affecting either total 1,25(OH)2D3 uptake or maximal 1,25(OH)2D3 -VDR binding .
0.9385 1.0000 1.0000 Microtubule disruption totally abolished the ability of exogenous 1,25(OH)2D3 to suppress its own synthesis and to induce 24-hydroxylase mRNA and activity, without affecting either total 1,25(OH)2D3 uptake or maximal 1,25(OH)2D3 protein-VDR binding .
1.5299 10.9936 0.9960 Microtubule disruption totally abolished the ability of exogenous 1,25(OH)2D3 to suppress its own synthesis and to induce protein24-hydroxylase mRNA and activity, without affecting either total 1,25(OH)2D3 uptake or maximal 1,25(OH)2D3 -VDR binding .
0.9666 1.0000 1.0000 proteinMicrotubule disruption totally abolished the ability of exogenous 1,25(OH)2D3 to suppress its own synthesis and to induce 24-hydroxylase mRNA and activity, without affecting either total 1,25(OH)2D3 uptake or maximal 1,25(OH)2D3 -VDR binding .
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1.7558 10.5349 1.0000 Thus, intact proteinmicrotubules are essential for 1,25(OH)2D3 -dependent modulation of gene transcription .
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4.1568 20.6865 10.9851 Interestingly, microtubule disruption also decreased monocyte 1,25(OH)2D3 synthesis , not by decreasing the Vmax of proteinmonocyte mitochondrial 1 alpha-hydroxylase but through an increase in the Km for 25(OH)2D3 .
0.9147 1.0000 1.0000 Interestingly, proteinmicrotubule disruption also decreased monocyte 1,25(OH)2D3 synthesis , not by decreasing the Vmax of monocyte mitochondrial 1 alpha-hydroxylase but through an increase in the Km for 25(OH)2D3 .
Interestingly, microtubule disruption also decreased cell_typemonocyte 1,25(OH)2D3 synthesis , not by decreasing the Vmax of monocyte mitochondrial 1 alpha-hydroxylase but through an increase in the Km for 25(OH)2D3 .
Interestingly, microtubule disruption also decreased monocyte 1,25(OH)2D3 synthesis , not by decreasing the Vmax of cell_typemonocyte mitochondrial 1 alpha-hydroxylase but through an increase in the Km for 25(OH)2D3 .
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0.9788 1.0000 1.0000 proteinMicrotubule disruption did not affect total cellular 25(OH)D3 uptake but reduced its intracellular trafficking to the mitochondria .
0.8068 1.0000 1.0000 Microtubule disruption did not affect total cellular 25(OH)D3 uptake but reduced its intracellular trafficking to the cell_typemitochondria .
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0.9330 1.0000 1.0000 Thus, proteinmicrotubules participate in intracellular 25(OH)D3 transport , and their integrity determines normal 1,25(OH)2D3 synthesis .
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1.6588 10.4889 1.0000 Relationship between Rap1 protein phosphorylation and regulation of Ca2+ transport in cell_typeplatelets : a new approach.
1.3920 10.6321 1.0000 Relationship between proteinRap1 protein phosphorylation and regulation of Ca2+ transport in platelets : a new approach.
1.7349 20.0048 0.9859 Relationship between proteinRap1 protein phosphorylation and regulation of Ca2+ transport in platelets : a new approach.
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1.8894 10.1389 1.0000 Although the interrelationship between the two messengers Ca2+ and cyclic AMP in cell_typeplatelet function is well documented, its mechanism of action still remains to be established.
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2.3706 20.6147 1.0000 We investigated here the question of the regulation of proteinplatelet Ca(2+)-ATPases by cyclic AMP through the phosphorylation of the Rap1 protein using a pathological model .
2.1383 20.8120 1.0000 We investigated here the question of the regulation of platelet Ca(2+)-ATPases by cyclic AMP through the phosphorylation of the proteinRap1 protein using a pathological model .
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2.1997 20.5441 1.0000 We first found experimental conditions where Ca(2+)-transport by platelet membrane vesicles appeared to be dependent on the phosphorylation of the proteinRap1 protein .
2.8041 20.9167 10.7596 We first found experimental conditions where Ca(2+)-transport by cell_typeplatelet membrane vesicles appeared to be dependent on the phosphorylation of the Rap1 protein .
1.8249 20.8977 0.9748 We first found experimental conditions where Ca(2+)-transport by platelet membrane vesicles appeared to be dependent on the phosphorylation of the proteinRap1 protein .
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6.2011 30.2549 10.7981 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the proteincyclic AMP -dependent protein kinase ( C. Sub. ).
4.7502 30.2965 10.8125 Then, we studied platelets of patients with congestive heart failure for their expression of the potential protein97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( C. Sub. ).
1.9901 20.4563 1.0000 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the proteinRap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( C. Sub. ).
1.9691 20.4964 1.0000 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the proteinRap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( C. Sub. ).
1.4863 10.4755 1.0000 Then, we studied cell_typeplatelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( C. Sub. ).
1.3793 10.7582 1.0000 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the proteincatalytic subunit of the cyclic AMP -dependent protein kinase ( C. Sub. ).
0.9112 1.0000 0.9861 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa proteinCa(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( C. Sub. ).
0.8479 0.9999 1.0000 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( proteinC. Sub. ).
0.6676 1.0000 0.9994 Then, we studied platelets of patients with congestive heart failure for their expression of the potential 97 kDa Ca(2+)-ATPase target of regulation through the Rap1 protein as well as the phosphorylation of the Rap1 protein using the catalytic subunit of the cyclic AMP -dependent protein kinase ( proteinC. Sub. ).
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3.9765 20.8541 10.8914 In the first patients studied, we found no significant modification in the expression of the 97 kDa Ca(2+)-ATPase by Western blotting using the proteinPL/IM 430 monoclonal antibody which specifically recognized this isoform.
3.6689 20.9933 10.4421 In the first patients studied, we found no significant modification in the expression of the protein97 kDa Ca(2+)-ATPase by Western blotting using the PL/IM 430 monoclonal antibody which specifically recognized this isoform.
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2.1877 20.9557 1.0000 In contrast, the proteinRap1 protein was differentially phosphorylated when using 15 micrograms/ml of the C. Sub.
1.6723 20.4825 0.9911 In contrast, the Rap1 protein was differentially phosphorylated when using 15 micrograms/ml of the proteinC. Sub.
1.8914 20.8851 0.9850 In contrast, the proteinRap1 protein was differentially phosphorylated when using 15 micrograms/ml of the C. Sub.
1.7728 20.1566 0.9935 In contrast, the Rap1 protein was differentially phosphorylated when using 15 micrograms/ml of the proteinC. Sub.
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2.3512 20.8414 1.0000 These results allowed us to use these pathological platelets to study the relationship between the expression of proteinRap1 protein and the regulation of Ca2+ transport by selecting a patient with severe heart failure .
2.4016 20.5501 0.9999 These results allowed us to use these cell_typepathological platelets to study the relationship between the expression of Rap1 protein and the regulation of Ca2+ transport by selecting a patient with severe heart failure .
2.2154 20.6465 0.9918 These results allowed us to use these pathological platelets to study the relationship between the expression of proteinRap1 protein and the regulation of Ca2+ transport by selecting a patient with severe heart failure .
These results allowed us to use these pathological cell_typeplatelets to study the relationship between the expression of Rap1 protein and the regulation of Ca2+ transport by selecting a patient with severe heart failure .
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2.4248 20.1884 1.0000 We could show a decrease in the expression as well as in the phosphorylation of proteinRap1 protein and demonstrate a lower effect of C. Sub. on Ca2+ transport .
1.6408 10.5014 1.0000 We could show a decrease in the expression as well as in the phosphorylation of Rap1 protein and demonstrate a lower effect of proteinC. Sub. on Ca2+ transport .
2.2279 20.5841 0.9918 We could show a decrease in the expression as well as in the phosphorylation of proteinRap1 protein and demonstrate a lower effect of C. Sub. on Ca2+ transport .
1.0947 10.8749 0.9892 We could show a decrease in the expression as well as in the phosphorylation of Rap1 protein and demonstrate a lower effect of proteinC. Sub. on Ca2+ transport .
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2.4384 20.1620 1.0000 Finally, by studying a further series of patients , we could confirm that the decrease in Rap1 protein expression in heart failure, whatever its extent, was variable, and could strictly correlate the expression of proteinRap1 protein with the stimulatory effect of C. Sub. on Ca2+ transport .
1.6909 10.2571 1.0000 Finally, by studying a further series of patients , we could confirm that the decrease in Rap1 protein expression in heart failure, whatever its extent, was variable, and could strictly correlate the expression of Rap1 protein with the stimulatory effect of proteinC. Sub. on Ca2+ transport .
1.5790 10.9845 1.0000 Finally, by studying a further series of patients , we could confirm that the decrease in proteinRap1 protein expression in heart failure, whatever its extent, was variable, and could strictly correlate the expression of Rap1 protein with the stimulatory effect of C. Sub. on Ca2+ transport .
2.4023 20.1193 0.9970 Finally, by studying a further series of patients , we could confirm that the decrease in proteinRap1 protein expression in heart failure, whatever its extent, was variable, and could strictly correlate the expression of Rap1 protein with the stimulatory effect of C. Sub. on Ca2+ transport .
2.3767 20.6147 0.9948 Finally, by studying a further series of patients , we could confirm that the decrease in Rap1 protein expression in heart failure, whatever its extent, was variable, and could strictly correlate the expression of proteinRap1 protein with the stimulatory effect of C. Sub. on Ca2+ transport .
1.1129 10.6462 0.9904 Finally, by studying a further series of patients , we could confirm that the decrease in Rap1 protein expression in heart failure, whatever its extent, was variable, and could strictly correlate the expression of Rap1 protein with the stimulatory effect of proteinC. Sub. on Ca2+ transport .
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2.3064 20.6228 1.0000 Besides the evidence for regulation of the expression of the Rap1 protein in platelets from patients with heart failure , these findings constitute a new approach in favour of the regulation of platelet Ca2+ transport through the phosphorylation of the proteinRap1 protein .
2.2814 20.7275 1.0000 Besides the evidence for regulation of the expression of the proteinRap1 protein in platelets from patients with heart failure , these findings constitute a new approach in favour of the regulation of platelet Ca2+ transport through the phosphorylation of the Rap1 protein .
1.8392 10.1807 1.0000 Besides the evidence for regulation of the expression of the Rap1 protein in cell_typeplatelets from patients with heart failure , these findings constitute a new approach in favour of the regulation of platelet Ca2+ transport through the phosphorylation of the Rap1 protein .
2.2197 20.9489 0.9901 Besides the evidence for regulation of the expression of the proteinRap1 protein in platelets from patients with heart failure , these findings constitute a new approach in favour of the regulation of platelet Ca2+ transport through the phosphorylation of the Rap1 protein .
2.1869 20.8622 0.9887 Besides the evidence for regulation of the expression of the Rap1 protein in platelets from patients with heart failure , these findings constitute a new approach in favour of the regulation of platelet Ca2+ transport through the phosphorylation of the proteinRap1 protein .
1.7823 10.3864 0.9999 Besides the evidence for regulation of the expression of the Rap1 protein in platelets from patients with heart failure , these findings constitute a new approach in favour of the regulation of cell_typeplatelet Ca2+ transport through the phosphorylation of the Rap1 protein .
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0.9121 1.0000 1.0000 An proteinIRF-1 -dependent pathway of DNA damage-induced apoptosis in mitogen-activated T lymphocytes .
3.5766 20.2038 10.5814 An IRF-1 -dependent pathway of DNA damage-induced apoptosis in cell_typemitogen-activated T lymphocytes .
An IRF-1 -dependent pathway of DNA damage-induced apoptosis in cell_linemitogen-activated T lymphocytes .
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0.8958 1.0000 1.0000 cell_typeLymphocytes are particularly susceptible to DNA damage-induced apoptosis , a response which may serve as a form of ' altruistic suicide ' to counter their intrinsic high potential for mutation and clonal expansion .
cell_lineLymphocytes are particularly susceptible to DNA damage-induced apoptosis , a response which may serve as a form of ' altruistic suicide ' to counter their intrinsic high potential for mutation and clonal expansion .
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3.0378 10.8904 10.1225 The proteintumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes , but an as yet unknown, p53 -independent pathway (s) appears to mediate the same event in mitogen-activated mature T lymphocytes .
1.5450 10.6779 1.0000 The tumour suppressor p53 has been shown to regulate this type of apoptosis in cell_typethymocytes , but an as yet unknown, p53 -independent pathway (s) appears to mediate the same event in mitogen-activated mature T lymphocytes .
0.8406 1.0000 1.0000 The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes , but an as yet unknown, proteinp53 -independent pathway (s) appears to mediate the same event in mitogen-activated mature T lymphocytes .
4.9975 30.6086 10.4708 The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes , but an as yet unknown, p53 -independent pathway (s) appears to mediate the same event in cell_typemitogen-activated mature T lymphocytes .
1.1170 0.9999 10.2637 The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes , but an as yet unknown, p53 -independent pathway (s) appears to mediate the same event in mitogen-activated mature cell_typeT lymphocytes .
The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes , but an as yet unknown, p53 -independent pathway (s) appears to mediate the same event in cell_linemitogen-activated mature T lymphocytes .
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1.8375 20.7036 0.9997 Here we show DNA damage-induced apoptosis in these cell_typeT lymphocytes is dependent on the antioncogenic transcription factor interferon regulatory factor (IRF)-1 .
5.6664 30.2026 20.3340 Here we show DNA damage-induced apoptosis in these T lymphocytes is dependent on the proteinantioncogenic transcription factor interferon regulatory factor (IRF)-1 .
2.6348 20.8646 10.8440 Here we show DNA damage-induced apoptosis in these T lymphocytes is dependent on the proteinantioncogenic transcription factor interferon regulatory factor (IRF)-1 .
Here we show DNA damage-induced apoptosis in these T lymphocytes is dependent on the antioncogenic transcription factor interferon regulatory factor protein(IRF)-1 .
Here we show DNA damage-induced apoptosis in these T lymphocytes is dependent on the proteinantioncogenic transcription factor interferon regulatory factor (IRF)-1 .
Here we show DNA damage-induced apoptosis in these T lymphocytes is dependent on the antioncogenic proteintranscription factor interferon regulatory factor (IRF)-1 .
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3.5278 20.9383 10.7902 Thus two different proteinanti-onco-genic transcription factors , p53 and IRF-1 , are required for distinct apoptotic pathways in T lymphocytes .
1.9704 20.9802 0.9998 Thus two different anti-onco-genic transcription factors , p53 and IRF-1 , are required for distinct apoptotic pathways in cell_typeT lymphocytes .
0.9390 1.0000 1.0000 Thus two different anti-onco-genic transcription factors , proteinp53 and IRF-1 , are required for distinct apoptotic pathways in T lymphocytes .
0.9219 1.0000 1.0000 Thus two different anti-onco-genic transcription factors , p53 and proteinIRF-1 , are required for distinct apoptotic pathways in T lymphocytes .
1.3411 1.0000 10.0341 Thus two different anti-onco-genic proteintranscription factors , p53 and IRF-1 , are required for distinct apoptotic pathways in T lymphocytes .
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4.9706 30.2348 20.8455 We also show that mitogen induction of the DNAinterleukin-1 beta converting enzyme ( ICE ) gene , a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3 , is IRF-1 -dependent .
3.8968 40.9729 10.5059 We also show that mitogen induction of the proteininterleukin-1 beta converting enzyme ( ICE ) gene , a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3 , is IRF-1 -dependent .
1.2990 0.9987 20.9183 We also show that mitogen induction of the interleukin-1 beta converting enzyme ( ICE ) gene , a mammalian homologue of the DNACaenorhabditis elegans cell death gene ced-3 , is IRF-1 -dependent .
0.9282 0.9998 0.9999 We also show that mitogen induction of the interleukin-1 beta converting enzyme ( ICE ) gene , a mammalian homologue of the Caenorhabditis elegans cell death gene DNAced-3 , is IRF-1 -dependent .
0.8507 1.0000 1.0000 We also show that mitogen induction of the interleukin-1 beta converting enzyme ( ICE ) gene , a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3 , is proteinIRF-1 -dependent .
0.8039 1.0000 0.9554 We also show that mitogen induction of the interleukin-1 beta converting enzyme ( DNAICE ) gene , a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3 , is IRF-1 -dependent .
We also show that mitogen induction of the interleukin-1 beta converting enzyme ( ICE ) gene , a proteinmammalian homologue of the Caenorhabditis elegans cell death gene ced-3 , is IRF-1 -dependent .
We also show that mitogen induction of the interleukin-1 beta converting enzyme ( proteinICE ) gene , a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3 , is IRF-1 -dependent .
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2.2029 20.2785 0.9999 Ectopic overexpression of IRF-1 results in the activation of the DNAendogenous gene for ICE and enhances the sensitivity of cells to radiation-induced apoptosis .
1.6320 10.8055 1.0000 Ectopic overexpression of proteinIRF-1 results in the activation of the endogenous gene for ICE and enhances the sensitivity of cells to radiation-induced apoptosis .
0.9550 1.0000 1.0000 Ectopic overexpression of IRF-1 results in the activation of the endogenous gene for DNAICE and enhances the sensitivity of cells to radiation-induced apoptosis .
Ectopic overexpression of IRF-1 results in the activation of the endogenous gene for proteinICE and enhances the sensitivity of cells to radiation-induced apoptosis .
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2.9371 10.8989 10.4352 Circadian rhythm of glucocorticoid receptors in cell_typehuman peripheral leukocytes and their reactivity to glucocorticoids .
1.9868 20.0590 0.9999 Circadian rhythm of proteinglucocorticoid receptors in human peripheral leukocytes and their reactivity to glucocorticoids .
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1.7571 10.6157 1.0000 1) There exists a CR of GR in human leukocytes , PMN , and cell_typemonocytes with the peak values from 0400 to 0800 hr and the trough values between 2300 and 0000 hr.
1.5965 10.3608 0.9999 1) There exists a CR of GR in cell_typehuman leukocytes , PMN , and monocytes with the peak values from 0400 to 0800 hr and the trough values between 2300 and 0000 hr.
0.9073 1.0000 1.0000 1) There exists a CR of proteinGR in human leukocytes , PMN , and monocytes with the peak values from 0400 to 0800 hr and the trough values between 2300 and 0000 hr.
0.9045 1.0000 1.0000 1) There exists a CR of GR in human leukocytes , cell_typePMN , and monocytes with the peak values from 0400 to 0800 hr and the trough values between 2300 and 0000 hr.
1.7489 10.3610 1.0000 1) There exists a proteinCR of GR in human leukocytes , PMN , and monocytes with the peak values from 0400 to 0800 hr and the trough values between 2300 and 0000 hr.
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1.7555 10.7939 1.0000 2) The FI of the chemotactic migration rate of cell_typePMN by cortisol also showed diurnal changes which were synchronous with that of GR .
1.7549 10.8190 1.0000 2) The FI of the chemotactic migration rate of PMN by cortisol also showed diurnal changes which were synchronous with that of proteinGR .
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0.9074 1.0000 1.0000 This indicates that the CR of proteinGR may be of functional significance.
0.8808 1.0000 1.0000 This indicates that the proteinCR of GR may be of functional significance.
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0.9502 1.0000 1.0000 3) In Cushing's syndrome , the CR of proteinGR was normal in spite of the fact that the CR of plasma cortisol was disturbed.
1.7372 10.5404 1.0000 3) In Cushing's syndrome , the CR of GR was normal in spite of the fact that the proteinCR of plasma cortisol was disturbed.
1.6801 10.5958 1.0000 3) In Cushing's syndrome , the proteinCR of GR was normal in spite of the fact that the CR of plasma cortisol was disturbed.
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0.9280 1.0000 1.0000 This indicates the independency of the CR of proteinGR from that of cortisol .
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0.9384 1.0000 1.0000 4) In apoplexy caused by brain ischemia , the CR of proteinGR was abolished in patients with basal lesions but preserved when the lesions were located in the cerebral cortex .
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1.7569 10.7166 1.0000 These results strongly suggest that the main " circadian pacemaker " of proteinGR is located in the basal brain , most probably in the suprachiasmatic nuclei as has been suggested for rodents .
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1.7124 0.9987 10.7850 cell_lineB-lymphoblastoid cell lines from multiple sclerosis patients and a healthy control producing a putative new human retrovirus and Epstein-Barr virus .
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3.9691 20.5251 10.4698 On several occasions we have observed retrovirus-like particles ( RVLPs ) by transmission electron microscopy ( EM ) of cell_linecultured T cells from a patient with MS .
0.6407 1.0000 1.0000 On several occasions we have observed retrovirus-like particles ( proteinRVLPs ) by transmission electron microscopy ( EM ) of cultured T cells from a patient with MS .
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4.0582 20.8695 10.8253 Later we established spontaneously formed cell_lineB-lymphoblastoid cell lines ( LCLs ) from a patient with an MS -like disease and from another patient with MS who had a reactivated Epstein-Barr virus (EBV) infection .
0.9681 1.0000 1.0000 Later we established spontaneously formed B-lymphoblastoid cell lines ( cell_lineLCLs ) from a patient with an MS -like disease and from another patient with MS who had a reactivated Epstein-Barr virus (EBV) infection .
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0.9157 0.9999 1.0000 Both cell_lineLCLs were found by EM to produce RVLP and EBV particles .
1.6923 10.0263 1.0000 Both LCLs were found by EM to produce proteinRVLP and EBV particles .
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1.6070 10.5103 1.0000 Reverse transcriptase (RT) assays were positive in purified viral material from both cell_lineLCLs .
0.9154 0.9999 0.9996 proteinReverse transcriptase (RT) assays were positive in purified viral material from both LCLs .
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1.8493 10.7188 1.0000 To substantiate these findings we initiated an intensified culturing procedure and were able to establish cell_lineLCLs from 5 out of 21 consecutive MS patients and 1 out of 13 consecutive healthy controls .
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0.9062 0.9999 1.0000 All cell_lineLCLs were found to produce both RVLP and EBV particles by EM .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.1292 30.9231 20.7003 Identification of an ionomycin /cyclosporin A -responsive element within the DNAhuman T cell receptor gamma enhancer .
4.5451 20.9656 20.7902 Identification of an DNAionomycin /cyclosporin A -responsive element within the human T cell receptor gamma enhancer .
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1.4992 10.9804 0.9998 Activation through the Ca2+ / calcineurin pathway is essential to the transcription of many DNAcytokine genes .
0.9592 1.0000 1.0000 Activation through the Ca2+ / proteincalcineurin pathway is essential to the transcription of many cytokine genes .
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1.5677 10.7079 1.0000 The conserved cis-acting sequence , GGAAAA , and proteintranscription factors binding to this sequence are involved in the response to increased intracellular Ca2+ concentrations .
2.3660 20.6325 0.9999 The conserved DNAcis-acting sequence , GGAAAA , and transcription factors binding to this sequence are involved in the response to increased intracellular Ca2+ concentrations .
The DNAconserved cis-acting sequence , GGAAAA , and transcription factors binding to this sequence are involved in the response to increased intracellular Ca2+ concentrations .
Cls_Score Left_Reg_Score Right_Reg_Score Text
7.6233 30.6218 20.6667 Here we report the identification and importance of the same sequence in a non-cytokine gene , the DNAhuman T cell receptor gamma ( TCRG ) enhancer .
1.7909 20.5857 0.9994 Here we report the identification and importance of the same sequence in a DNAnon-cytokine gene , the human T cell receptor gamma ( TCRG ) enhancer .
0.8359 1.0000 0.9651 Here we report the identification and importance of the same sequence in a non-cytokine gene , the human T cell receptor gamma ( proteinTCRG ) enhancer .
Here we report the identification and importance of the same sequence in a non-cytokine gene , the proteinhuman T cell receptor gamma ( TCRG ) enhancer .
Here we report the identification and importance of the same sequence in a non-cytokine gene , the cell_typehuman T cell receptor gamma ( TCRG ) enhancer .
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2.4270 20.2505 0.9999 Results from site-directed mutations and electrophoretic mobility shift assays strongly suggest that this sequence mediates the ionomycin -induced activation of the DNATCRG enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7885 10.7459 1.0000 Our studies provide an explanation for a previous observation that RNATCRG mRNA levels , but not mRNA levels for T cell receptor alpha and -beta , are increased by ionomycin treatment .
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1.9735 20.5005 0.8207 Coexpression of proteinNF-kappa B /Rel and Sp1 transcription factors in human immunodeficiency virus 1 -induced, dendritic cell-T-cell syncytia .
1.3022 20.8616 0.9996 Coexpression of proteinNF-kappa B /Rel and Sp1 transcription factors in human immunodeficiency virus 1 -induced, dendritic cell-T-cell syncytia .
0.8364 0.9926 1.0000 Coexpression of NF-kappa B /Rel and Sp1 proteintranscription factors in human immunodeficiency virus 1 -induced, dendritic cell-T-cell syncytia .
0.7886 0.9984 1.0000 Coexpression of NF-kappa B /Rel and proteinSp1 transcription factors in human immunodeficiency virus 1 -induced, dendritic cell-T-cell syncytia .
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2.4090 20.7631 0.9999 Productive infection of cell_typeT cells with human immunodeficiency virus 1 ( HIV-1 ) typically requires that the T cells be stimulated with antigens or mitogens .
2.4023 20.2945 0.9999 Productive infection of T cells with human immunodeficiency virus 1 ( HIV-1 ) typically requires that the cell_typeT cells be stimulated with antigens or mitogens .
0.8762 1.0000 1.0000 Productive infection of T cells with human immunodeficiency virus 1 ( HIV-1 ) typically requires that the T cells be stimulated with proteinantigens or mitogens .
0.8355 0.9998 1.0000 Productive infection of T cells with human immunodeficiency virus 1 ( HIV-1 ) typically requires that the T cells be stimulated with antigens or proteinmitogens .
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1.3264 10.9676 0.9998 This requirement has been attributed to the activation of the transcription factor NF-kappa B , which synergizes with the constitutive transcription factor Sp1 to drive the DNAHIV-1 promoter .
1.2859 10.7156 0.9989 This requirement has been attributed to the activation of the proteintranscription factor NF-kappa B , which synergizes with the constitutive transcription factor Sp1 to drive the HIV-1 promoter .
0.9324 0.9999 1.0000 This requirement has been attributed to the activation of the transcription factor NF-kappa B , which synergizes with the constitutive transcription factor proteinSp1 to drive the HIV-1 promoter .
0.9088 0.9993 1.0000 This requirement has been attributed to the activation of the transcription factor proteinNF-kappa B , which synergizes with the constitutive transcription factor Sp1 to drive the HIV-1 promoter .
3.7784 20.6583 10.8158 This requirement has been attributed to the activation of the transcription factor NF-kappa B , which synergizes with the proteinconstitutive transcription factor Sp1 to drive the HIV-1 promoter .
This requirement has been attributed to the activation of the transcription factor NF-kappa B , which synergizes with the proteinconstitutive transcription factor Sp1 to drive the HIV-1 promoter .
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1.3470 10.8696 0.9998 Recently, we have found that vigorous replication of HIV-1 takes place in nonactivated memory T cells after syncytium formation with cell_typedendritic cells ( DCs ).
0.9010 1.0000 0.9999 Recently, we have found that vigorous replication of HIV-1 takes place in nonactivated memory T cells after syncytium formation with dendritic cells ( cell_typeDCs ).
4.6810 20.8144 10.7499 Recently, we have found that vigorous replication of HIV-1 takes place in cell_typenonactivated memory T cells after syncytium formation with dendritic cells ( DCs ).
Recently, we have found that vigorous replication of HIV-1 takes place in nonactivated cell_typememory T cells after syncytium formation with dendritic cells ( DCs ).
Recently, we have found that vigorous replication of HIV-1 takes place in nonactivated memory cell_typeT cells after syncytium formation with dendritic cells ( DCs ).
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2.1111 20.0912 0.9997 These syncytia lack cell_typeactivated cells as determined by an absence of staining for Ki-67 cell cycle antigen.
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1.6560 10.3079 1.0000 The expression and activity of NF-kappa B and proteinSp1 were, therefore, analyzed in isolated T cells and DCs from humans and mice .
1.4195 10.8978 1.0000 The expression and activity of proteinNF-kappa B and Sp1 were, therefore, analyzed in isolated T cells and DCs from humans and mice .
0.8780 0.9999 0.9999 The expression and activity of NF-kappa B and Sp1 were, therefore, analyzed in isolated T cells and cell_typeDCs from humans and mice .
4.3261 20.3656 10.5863 The expression and activity of NF-kappa B and Sp1 were, therefore, analyzed in cell_typeisolated T cells and DCs from humans and mice .
The expression and activity of NF-kappa B and Sp1 were, therefore, analyzed in isolated cell_typeT cells and DCs from humans and mice .
Cls_Score Left_Reg_Score Right_Reg_Score Text
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2.0362 20.1092 0.9999 T cells lack active proteinNF-kappa B but express Sp1 as expected.
1.3193 10.6755 1.0000 T cells lack active NF-kappa B but express proteinSp1 as expected.
0.8475 0.9979 0.9997 cell_typeT cells lack active NF-kappa B but express Sp1 as expected.
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2.1746 20.1614 1.0000 DCs express high levels of all known proteinNF-kappa B and Rel proteins , with activity residing primarily within RelB , p50 , and p65 .
1.5693 10.8203 1.0000 DCs express high levels of all known NF-kappa B and Rel proteins , with activity residing primarily within RelB , p50 , and proteinp65 .
1.4977 10.9606 0.9999 DCs express high levels of all known NF-kappa B and proteinRel proteins , with activity residing primarily within RelB , p50 , and p65 .
1.4619 10.9508 1.0000 DCs express high levels of all known NF-kappa B and Rel proteins , with activity residing primarily within proteinRelB , p50 , and p65 .
0.9444 1.0000 1.0000 cell_typeDCs express high levels of all known NF-kappa B and Rel proteins , with activity residing primarily within RelB , p50 , and p65 .
0.9177 1.0000 1.0000 DCs express high levels of all known NF-kappa B and Rel proteins , with activity residing primarily within RelB , proteinp50 , and p65 .
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0.9333 1.0000 0.9999 However, DCs lack Sp1 , which may explain the failure of HIV-1 to replicate in purified cell_typeDCs .
0.8951 0.9998 1.0000 However, cell_typeDCs lack Sp1 , which may explain the failure of HIV-1 to replicate in purified DCs .
0.8436 0.9999 1.0000 However, DCs lack proteinSp1 , which may explain the failure of HIV-1 to replicate in purified DCs .
1.8851 20.2806 0.9998 However, DCs lack Sp1 , which may explain the failure of HIV-1 to replicate in cell_typepurified DCs .
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2.2705 20.1715 1.0000 Coexpression of proteinNF-kappa B and Sp1 occurs in the heterologous DC-T-cell syncytia that are induced by HIV-1 .
1.6610 10.1191 1.0000 Coexpression of NF-kappa B and proteinSp1 occurs in the heterologous DC-T-cell syncytia that are induced by HIV-1 .
Coexpression of NF-kappa B and Sp1 occurs in the cell_typeheterologous DC-T-cell syncytia that are induced by HIV-1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9286 0.9999 1.0000 Since cell_typeDCs and memory T cells frequently traffic together in situ, these unusual heterologous syncytia could develop in infected individuals and lead to chronic HIV-1 replication without ostensible immune stimulation .
4.1556 20.1924 10.8054 Since DCs and cell_typememory T cells frequently traffic together in situ, these unusual heterologous syncytia could develop in infected individuals and lead to chronic HIV-1 replication without ostensible immune stimulation .
Since DCs and memory cell_typeT cells frequently traffic together in situ, these unusual heterologous syncytia could develop in infected individuals and lead to chronic HIV-1 replication without ostensible immune stimulation .
Since DCs and memory T cells frequently traffic together in situ, these unusual cell_typeheterologous syncytia could develop in infected individuals and lead to chronic HIV-1 replication without ostensible immune stimulation .
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3.6784 20.9210 10.6669 Cupric ion blocks NF kappa B activation through inhibiting the signal-induced phosphorylation of proteinI kappa B alpha .
3.3733 20.9257 10.5312 Cupric ion blocks proteinNF kappa B activation through inhibiting the signal-induced phosphorylation of I kappa B alpha .
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2.1724 20.1480 0.9999 A transcription factor NF kappa B , which regulates expression of various cellular genes involved in immune responses and DNAviral genes including HIV , is sequestered in the cytoplasm as a complex with an inhibitory protein I kappa B .
1.6432 0.9265 10.4954 A transcription factor proteinNF kappa B , which regulates expression of various cellular genes involved in immune responses and viral genes including HIV , is sequestered in the cytoplasm as a complex with an inhibitory protein I kappa B .
1.4738 10.4953 0.9991 A proteintranscription factor NF kappa B , which regulates expression of various cellular genes involved in immune responses and viral genes including HIV , is sequestered in the cytoplasm as a complex with an inhibitory protein I kappa B .
2.1438 20.6289 0.9999 A transcription factor NF kappa B , which regulates expression of various DNAcellular genes involved in immune responses and viral genes including HIV , is sequestered in the cytoplasm as a complex with an inhibitory protein I kappa B .
1.6250 10.3912 0.9996 A transcription factor NF kappa B , which regulates expression of various cellular genes involved in immune responses and viral genes including HIV , is sequestered in the cytoplasm as a complex with an inhibitory protein proteinI kappa B .
A transcription factor NF kappa B , which regulates expression of various cellular genes involved in immune responses and viral genes including HIV , is sequestered in the cytoplasm as a complex with an proteininhibitory protein I kappa B .
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3.6945 20.9418 10.6257 Various extracellular signals induce phosphorylation and rapid degradation of proteinI kappa B alpha to release NF kappa B .
3.3207 20.3583 10.8974 Various extracellular signals induce phosphorylation and rapid degradation of I kappa B alpha to release proteinNF kappa B .
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2.8402 20.6145 10.5562 Cu2+ was found to inhibit the activation of proteinNF kappa B induced by TNF-alpha , TPA , or H2O2 .
1.7057 10.2790 1.0000 Cu2+ was found to inhibit the activation of NF kappa B induced by proteinTNF-alpha , TPA , or H2O2 .
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4.0304 20.4665 10.6853 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from proteinI kappa B alpha , indicating that Cu2+ interferes with the dissociation of the NF kappa B -I kappa B complex .
3.7831 30.2539 10.2558 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from I kappa B alpha , indicating that Cu2+ interferes with the dissociation of the proteinNF kappa B -I kappa B complex .
3.3485 30.1163 10.3878 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of proteinNF kappa B from I kappa B alpha , indicating that Cu2+ interferes with the dissociation of the NF kappa B -I kappa B complex .
3.0962 30.9119 10.0663 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from I kappa B alpha , indicating that Cu2+ interferes with the dissociation of the proteinNF kappa B -I kappa B complex .
1.4820 10.6986 1.0000 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by proteinTNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from I kappa B alpha , indicating that Cu2+ interferes with the dissociation of the NF kappa B -I kappa B complex .
1.4938 0.9788 10.8480 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from I kappa B alpha , indicating that Cu2+ interferes with the dissociation of the NF kappa B protein-I kappa B complex .
0.5443 0.9959 10.5145 Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from I kappa B alpha , indicating that Cu2+ interferes with the dissociation of the NF kappa B protein-I kappa B complex .
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3.7526 20.8754 10.9517 Neither phosphorylation nor degradation of proteinI kappa B alpha was observed upon TNF-alpha stimulation in the presence of Cu2+ .
0.8165 0.9999 1.0000 Neither phosphorylation nor degradation of I kappa B alpha was observed upon proteinTNF-alpha stimulation in the presence of Cu2+ .
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3.9079 20.6526 10.9200 These results indicate that Cu2+ inhibits the release of NF kappa B by blockade of a signal leading to the phosphorylation of proteinI kappa B alpha .
3.6133 20.9090 10.4658 These results indicate that Cu2+ inhibits the release of proteinNF kappa B by blockade of a signal leading to the phosphorylation of I kappa B alpha .
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1.3446 10.6129 0.9999 Cloning a DNAcDNA from human NK/ T cells which codes for a protein with high proline content .
4.5607 20.4585 20.2222 Cloning a cDNA from cell_typehuman NK/ T cells which codes for a protein with high proline content .
Cloning a cDNA from human cell_typeNK/ T cells which codes for a protein with high proline content .
Cloning a cDNA from human NK/ cell_typeT cells which codes for a protein with high proline content .
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6.9343 30.4269 20.6243 A cDNA clone , B4-2 , was isolated from a DNAnatural killer (NK) minus T cell subtractive library .
1.6159 10.0329 1.0000 A cDNA clone , DNAB4-2 , was isolated from a natural killer (NK) minus T cell subtractive library .
1.2952 10.3800 0.9999 A DNAcDNA clone , B4-2 , was isolated from a natural killer (NK) minus T cell subtractive library .
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1.7706 10.3864 1.0000 The B4-2 clone coded for an RNAmRNA of 2061 bp in length.
1.5721 10.3350 1.0000 The DNAB4-2 clone coded for an mRNA of 2061 bp in length.
The DNAB4-2 clone coded for an mRNA of 2061 bp in length.
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3.0275 10.9792 10.7234 It encodes a deduced protein327 aa protein with a calculated molecular mass of 35.2 kDa.
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1.5532 10.8750 0.9999 Searching of DNAB4-2 DNA and protein sequences against various databases revealed no high homology to other sequences.
1.4792 10.7005 0.9999 Searching of B4-2 DNA and DNAprotein sequences against various databases revealed no high homology to other sequences.
Searching of DNAB4-2 DNA and protein sequences against various databases revealed no high homology to other sequences.
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4.2953 20.9630 10.8229 However, B4-2 has an unusually high proline content (13%), contains a putative nuclear targeting sequence , and has several SPXX motifs which are frequently found in proteingene regulatory proteins .
2.1818 20.1819 1.0000 However, B4-2 has an unusually high proline content (13%), contains a putative nuclear targeting sequence , and has several proteinSPXX motifs which are frequently found in gene regulatory proteins .
1.5044 10.0621 10.6033 However, B4-2 has an unusually high proline content (13%), contains a putative proteinnuclear targeting sequence , and has several SPXX motifs which are frequently found in gene regulatory proteins .
0.8835 0.9999 1.0000 However, proteinB4-2 has an unusually high proline content (13%), contains a putative nuclear targeting sequence , and has several SPXX motifs which are frequently found in gene regulatory proteins .
However, DNAB4-2 has an unusually high proline content (13%), contains a putative nuclear targeting sequence , and has several SPXX motifs which are frequently found in gene regulatory proteins .
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1.5609 10.7171 0.9999 One of the stretches of prolines in B4-2 closely resembles the ligand for proteins with proteinSH3 domains .
1.5659 10.7648 1.0000 One of the stretches of prolines in proteinB4-2 closely resembles the ligand for proteins with SH3 domains .
One of the stretches of prolines in DNAB4-2 closely resembles the ligand for proteins with SH3 domains .
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3.8098 20.8841 10.4927 Northern hybridization data showed that B4-2 is not a lymphoid specific gene and is expressed in a cell_linehepatoma cell line and also weakly transcribed or absent in a variety of other cells.
3.6838 20.8914 10.5241 Northern hybridization data showed that B4-2 is not a DNAlymphoid specific gene and is expressed in a hepatoma cell line and also weakly transcribed or absent in a variety of other cells.
1.6144 10.3632 1.0000 Northern hybridization data showed that proteinB4-2 is not a lymphoid specific gene and is expressed in a hepatoma cell line and also weakly transcribed or absent in a variety of other cells.
Northern hybridization data showed that DNAB4-2 is not a lymphoid specific gene and is expressed in a hepatoma cell line and also weakly transcribed or absent in a variety of other cells.
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3.4760 20.2480 10.7972 A polyclonal antiserum raised against recombinant B4-2 recognizes a protein32-34 kDa protein in lymphocytes .
1.8311 20.4640 0.9999 A polyclonal antiserum raised against proteinrecombinant B4-2 recognizes a 32-34 kDa protein in lymphocytes .
1.6668 10.0834 0.9999 A polyclonal antiserum raised against recombinant B4-2 recognizes a 32-34 kDa protein in cell_typelymphocytes .
0.9218 1.0000 1.0000 A polyclonal antiserum raised against recombinant proteinB4-2 recognizes a 32-34 kDa protein in lymphocytes .
A polyclonal antiserum raised against recombinant DNAB4-2 recognizes a 32-34 kDa protein in lymphocytes .
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2.7721 20.8773 10.1383 Activation of JAK3 , but not JAK1 , is critical for IL-2 -induced proliferation and STAT5 recruitment by a COOH-terminal region of the proteinIL-2 receptor beta-chain .
2.1033 20.9442 0.9999 Activation of JAK3 , but not JAK1 , is critical for IL-2 -induced proliferation and STAT5 recruitment by a proteinCOOH-terminal region of the IL-2 receptor beta-chain .
1.5236 10.9394 1.0000 Activation of proteinJAK3 , but not JAK1 , is critical for IL-2 -induced proliferation and STAT5 recruitment by a COOH-terminal region of the IL-2 receptor beta-chain .
1.5229 10.3765 1.0000 Activation of JAK3 , but not proteinJAK1 , is critical for IL-2 -induced proliferation and STAT5 recruitment by a COOH-terminal region of the IL-2 receptor beta-chain .
0.8947 1.0000 1.0000 Activation of JAK3 , but not JAK1 , is critical for proteinIL-2 -induced proliferation and STAT5 recruitment by a COOH-terminal region of the IL-2 receptor beta-chain .
0.8810 1.0000 1.0000 Activation of JAK3 , but not JAK1 , is critical for IL-2 -induced proliferation and proteinSTAT5 recruitment by a COOH-terminal region of the IL-2 receptor beta-chain .
1.9123 20.5235 0.9921 Activation of JAK3 , but not JAK1 , is critical for IL-2 -induced proliferation and STAT5 recruitment by a COOH-terminal region of the proteinIL-2 receptor beta-chain .
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1.6567 10.3953 1.0000 A number of cytokines and growth factors use the proteinJAK -STAT pathway to signal from the cell membrane to the nucleus .
1.6389 10.7654 1.0000 A number of proteincytokines and growth factors use the JAK -STAT pathway to signal from the cell membrane to the nucleus .
1.5397 10.9072 0.9999 A number of cytokines and proteingrowth factors use the JAK -STAT pathway to signal from the cell membrane to the nucleus .
0.9597 1.0000 1.0000 A number of cytokines and growth factors use the JAK protein-STAT pathway to signal from the cell membrane to the nucleus .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1180 10.7568 10.9746 While proteinhomodimerizing cytokine receptors may transmit signal via a single form of JAK (i.e. growth hormone receptors ), several multicomponent cytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. interferon receptors ).
3.0631 10.6178 10.3484 While homodimerizing cytokine receptors may transmit signal via a single form of JAK (i.e. proteingrowth hormone receptors ), several multicomponent cytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. interferon receptors ).
2.1027 20.0503 1.0000 While homodimerizing cytokine receptors may transmit signal via a single form of JAK (i.e. growth hormone receptors ), several multicomponent cytokine receptors have been shown to require simultaneous activation of pairs of different proteinJAK kinases (i.e. interferon receptors ).
2.0731 10.4244 10.7205 While homodimerizing cytokine receptors may transmit signal via a single form of JAK (i.e. growth hormone receptors ), several proteinmulticomponent cytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. interferon receptors ).
1.5748 10.6239 1.0000 While homodimerizing cytokine receptors may transmit signal via a single form of proteinJAK (i.e. growth hormone receptors ), several multicomponent cytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. interferon receptors ).
1.5218 10.4400 0.9998 While homodimerizing cytokine receptors may transmit signal via a single form of JAK (i.e. growth hormone receptors ), several multicomponent cytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. proteininterferon receptors ).
1.0877 1.0000 10.0160 While homodimerizing proteincytokine receptors may transmit signal via a single form of JAK (i.e. growth hormone receptors ), several multicomponent cytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. interferon receptors ).
0.6962 0.9998 1.0000 While homodimerizing cytokine receptors may transmit signal via a single form of JAK (i.e. growth hormone receptors ), several multicomponent proteincytokine receptors have been shown to require simultaneous activation of pairs of different JAK kinases (i.e. interferon receptors ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6611 10.4841 1.0000 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( proteinIL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
1.5804 10.5026 1.0000 Recent evidence for a preferential coupling of proteinJAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
1.5664 10.3348 1.0000 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to proteinIL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
1.5385 10.6031 1.0000 Recent evidence for a preferential coupling of JAK3 to proteininterleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
0.9262 1.0000 1.0000 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and proteinJAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
0.9228 1.0000 1.0000 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and proteinJAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
0.9150 1.0000 1.0000 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by proteinIL-2 -induced heterodimerization of their receptor partners .
0.8352 0.9999 1.0000 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of proteinJAK1 and JAK3 caused by IL-2 -induced heterodimerization of their receptor partners .
1.3793 10.8138 0.9999 Recent evidence for a preferential coupling of JAK3 to interleukin-2 receptor-gamma ( IL-2R gamma ) and JAK1 to IL-2R beta supports the concept of heterotrans-activation of JAK1 and JAK3 caused by IL-2 -induced heterodimerization of their proteinreceptor partners .
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5.0543 30.5239 10.6649 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of JAK1 and JAK3 , but demonstrated that IL-2 stimulated JAK3 to a significantly larger extent than JAK1 in human T lymphocytes and the cell_lineYT cell line .
2.1939 20.6922 0.9997 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of JAK1 and JAK3 , but demonstrated that IL-2 stimulated JAK3 to a significantly larger extent than JAK1 in cell_typehuman T lymphocytes and the YT cell line .
1.6485 10.1193 1.0000 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of JAK1 and JAK3 , but demonstrated that proteinIL-2 stimulated JAK3 to a significantly larger extent than JAK1 in human T lymphocytes and the YT cell line .
1.5940 10.5655 1.0000 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of JAK1 and JAK3 , but demonstrated that IL-2 stimulated JAK3 to a significantly larger extent than proteinJAK1 in human T lymphocytes and the YT cell line .
1.5930 10.1344 1.0000 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of proteinJAK1 and JAK3 , but demonstrated that IL-2 stimulated JAK3 to a significantly larger extent than JAK1 in human T lymphocytes and the YT cell line .
1.5105 10.8826 1.0000 The present study verified the ability of proteinIL-2 to cause tyrosine phosphorylation and activation of JAK1 and JAK3 , but demonstrated that IL-2 stimulated JAK3 to a significantly larger extent than JAK1 in human T lymphocytes and the YT cell line .
0.9029 1.0000 1.0000 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of JAK1 and proteinJAK3 , but demonstrated that IL-2 stimulated JAK3 to a significantly larger extent than JAK1 in human T lymphocytes and the YT cell line .
0.8640 1.0000 1.0000 The present study verified the ability of IL-2 to cause tyrosine phosphorylation and activation of JAK1 and JAK3 , but demonstrated that IL-2 stimulated proteinJAK3 to a significantly larger extent than JAK1 in human T lymphocytes and the YT cell line .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9518 20.2022 10.9439 This conclusion was based upon several independent criteria, including more vigorous tyrosine phosphorylation of JAK3 , more marked enzymatic activation of JAK3 as well as higher abundance of JAK3 in activated proteinIL-2 receptor complexes .
1.5673 10.6202 1.0000 This conclusion was based upon several independent criteria, including more vigorous tyrosine phosphorylation of JAK3 , more marked enzymatic activation of JAK3 as well as higher abundance of proteinJAK3 in activated IL-2 receptor complexes .
1.5638 10.4723 1.0000 This conclusion was based upon several independent criteria, including more vigorous tyrosine phosphorylation of JAK3 , more marked enzymatic activation of proteinJAK3 as well as higher abundance of JAK3 in activated IL-2 receptor complexes .
1.5474 10.6729 1.0000 This conclusion was based upon several independent criteria, including more vigorous tyrosine phosphorylation of proteinJAK3 , more marked enzymatic activation of JAK3 as well as higher abundance of JAK3 in activated IL-2 receptor complexes .
1.4420 10.6032 0.9965 This conclusion was based upon several independent criteria, including more vigorous tyrosine phosphorylation of JAK3 , more marked enzymatic activation of JAK3 as well as higher abundance of JAK3 in activated proteinIL-2 receptor complexes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2487 20.6622 10.9973 Furthermore, when proteinhuman IL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or TYK2 .
3.7368 20.7609 10.8564 Furthermore, when human IL-2R beta was stably expressed in cell_linemurine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or TYK2 .
1.6005 10.3152 1.0000 Furthermore, when human IL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either proteinJAK1 , JAK2 or TYK2 .
1.5387 10.1922 1.0000 Furthermore, when human IL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and proteinJAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or TYK2 .
0.9288 1.0000 1.0000 Furthermore, when human IL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , proteinJAK2 or TYK2 .
0.8999 1.0000 1.0000 Furthermore, when human IL-2R beta was stably expressed in murine BA/F3 cells , robust proteinIL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or TYK2 .
0.8705 1.0000 1.0000 Furthermore, when human IL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or proteinTYK2 .
0.5178 0.9997 0.9998 Furthermore, when human proteinIL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or TYK2 .
Furthermore, when human proteinIL-2R beta was stably expressed in murine BA/F3 cells , robust IL-2 -induced proliferation and JAK3 activation occurred without detectable involvement of either JAK1 , JAK2 or TYK2 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3184 20.1856 1.0000 We therefore propose that proteinIL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and JAK3 following IL-2 -induced heterodimerization of IL-2R beta and IL-2R gamma .
1.6006 10.8034 0.9999 We therefore propose that IL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and JAK3 following IL-2 -induced heterodimerization of IL-2R beta and proteinIL-2R gamma .
1.5716 10.5414 1.0000 We therefore propose that IL-2 receptor signal transduction does not depend on equimolar heterodimerization of proteinJAK1 and JAK3 following IL-2 -induced heterodimerization of IL-2R beta and IL-2R gamma .
1.4830 10.9901 1.0000 We therefore propose that IL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and JAK3 following IL-2 -induced heterodimerization of proteinIL-2R beta and IL-2R gamma .
0.9521 1.0000 1.0000 We therefore propose that IL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and JAK3 following proteinIL-2 -induced heterodimerization of IL-2R beta and IL-2R gamma .
0.9194 1.0000 1.0000 We therefore propose that IL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and proteinJAK3 following IL-2 -induced heterodimerization of IL-2R beta and IL-2R gamma .
We therefore propose that IL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and JAK3 following IL-2 -induced heterodimerization of proteinIL-2R beta and IL-2R gamma .
We therefore propose that proteinIL-2 receptor signal transduction does not depend on equimolar heterodimerization of JAK1 and JAK3 following IL-2 -induced heterodimerization of IL-2R beta and IL-2R gamma .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5790 20.6301 10.6120 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated proteinIL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
2.2253 20.1536 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the proteinreceptor complex relies on both IL-2R beta and IL-2R gamma .
2.1916 20.3047 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both proteinIL-2R beta and IL-2R gamma .
2.1574 20.1549 0.9999 Nonetheless, a proteinmembrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
2.0040 20.6986 0.9958 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated proteinIL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
1.6066 10.1980 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of proteinJAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
1.6048 10.5732 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and proteinIL-2R gamma .
1.5450 10.4592 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of proteinJAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
0.8919 1.0000 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( Asn240-Leu335 ) was critical for proteinJAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
0.7345 1.0000 0.9999 Nonetheless, a membrane-proximal region of human proteinIL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
0.6125 1.0000 1.0000 Nonetheless, a membrane-proximal region of human IL-2R beta ( proteinAsn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
3.0650 10.4235 10.4947 Nonetheless, a membrane-proximal region of proteinhuman IL-2R beta ( Asn240-Leu335 ) was critical for JAK3 activation, and the amount of JAK3 present in activated IL-2 receptor complexes increased with time, suggesting that stabilization of JAK3 binding to the receptor complex relies on both IL-2R beta and IL-2R gamma .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9177 20.5613 10.2019 Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in cell_typehuman T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
2.8015 20.8865 10.2779 Moreover, STAT5 was found to be the predominant proteinSTAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
2.1172 20.1778 1.0000 Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a proteinCOOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
2.1017 20.6146 1.0000 Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of proteinIL-2R gamma or JAK3 .
1.5280 10.7667 1.0000 Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of proteinIL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
0.9263 1.0000 1.0000 Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while proteinSTAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
0.9182 1.0000 1.0000 Moreover, proteinSTAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
0.8451 0.9999 1.0000 Moreover, STAT5 was found to be the predominant STAT transcription factor used by proteinIL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
0.8294 1.0000 1.0000 Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or proteinJAK3 .
Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human T cells , and specifically required a COOH-terminal region of IL-2R beta ( proteinSer386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
Moreover, STAT5 was found to be the predominant STAT transcription factor used by IL-2 in human cell_typeT cells , and specifically required a COOH-terminal region of IL-2R beta ( Ser386-Val525 ), while STAT5 recruitment was not correlated to activation of IL-2R gamma or JAK3 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9431 20.4677 10.8822 Up-regulation of high-affinity dehydroepiandrosterone binding activity by dehydroepiandrosterone in cell_typeactivated human T lymphocytes .
Up-regulation of high-affinity dehydroepiandrosterone binding activity by dehydroepiandrosterone in activated cell_typehuman T lymphocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1324 40.8728 20.4156 DHEA binding sites were examined using a whole-cell binding assay in a cell_linehuman T lymphoid cell line , PEER , revealing that a single class of high-affinity binding sites for DHEA (dissociation constant = 7.4 +/- 0.53 nmol/L, mean +/- SE, n = 4) was greatly increased when treated with DHEA , phorbol-12-myristate-13-acetate , and the Ca2+ ionophore A23187.
0.9329 1.0000 1.0000 DHEA binding sites were examined using a whole-cell binding assay in a human T lymphoid cell line , cell_linePEER , revealing that a single class of high-affinity binding sites for DHEA (dissociation constant = 7.4 +/- 0.53 nmol/L, mean +/- SE, n = 4) was greatly increased when treated with DHEA , phorbol-12-myristate-13-acetate , and the Ca2+ ionophore A23187.
2.8528 40.0453 10.0345 DHEA binding sites were examined using a whole-cell binding assay in a human T lymphoid cell line , PEER , revealing that a single class of proteinhigh-affinity binding sites for DHEA (dissociation constant = 7.4 +/- 0.53 nmol/L, mean +/- SE, n = 4) was greatly increased when treated with DHEA , phorbol-12-myristate-13-acetate , and the Ca2+ ionophore A23187.
0.7758 0.9900 0.9996 proteinDHEA binding sites were examined using a whole-cell binding assay in a human T lymphoid cell line , PEER , revealing that a single class of high-affinity binding sites for DHEA (dissociation constant = 7.4 +/- 0.53 nmol/L, mean +/- SE, n = 4) was greatly increased when treated with DHEA , phorbol-12-myristate-13-acetate , and the Ca2+ ionophore A23187.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5337 20.3779 1.0000 These results not only indicate the existence of a DHEA receptor , but also suggest that cell_typeT cells become susceptible to regulation by DHEA during the process of signal-induced activation .
2.1469 20.3404 1.0000 These results not only indicate the existence of a proteinDHEA receptor , but also suggest that T cells become susceptible to regulation by DHEA during the process of signal-induced activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6602 20.6569 0.9903 Ubiquitin-mediated processing of proteinNF-kappa B transcriptional activator precursor p105 .
0.9151 0.9995 0.9999 Ubiquitin-mediated processing of NF-kappa B transcriptional activator precursor proteinp105 .
2.5280 20.7530 10.0812 Ubiquitin-mediated processing of proteinNF-kappa B transcriptional activator precursor p105 .
Ubiquitin-mediated processing of NF-kappa B proteintranscriptional activator precursor p105 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2358 20.0965 1.0000 Reconstitution of a cell-free system and identification of the ubiquitin-carrier protein , E2 , and a novel proteinubiquitin-protein ligase , E3 , involved in conjugation.
2.2023 20.1185 1.0000 Reconstitution of a cell-free system and identification of the proteinubiquitin-carrier protein , E2 , and a novel ubiquitin-protein ligase , E3 , involved in conjugation.
0.9590 1.0000 1.0000 Reconstitution of a cell-free system and identification of the ubiquitin-carrier protein , proteinE2 , and a novel ubiquitin-protein ligase , E3 , involved in conjugation.
0.9511 1.0000 1.0000 Reconstitution of a cell-free system and identification of the ubiquitin-carrier protein , E2 , and a novel ubiquitin-protein ligase , proteinE3 , involved in conjugation.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1813 20.5265 0.9997 In most cases, the proteintranscriptional factor NF-kappa B is a heterodimer consisting of two subunits, p50 and p65 , which are encoded by two distinct genes of the Rel family .
1.7577 10.0182 1.0000 In most cases, the transcriptional factor NF-kappa B is a proteinheterodimer consisting of two subunits, p50 and p65 , which are encoded by two distinct genes of the Rel family .
0.9745 1.0000 1.0000 In most cases, the transcriptional factor NF-kappa B is a heterodimer consisting of two subunits, p50 and proteinp65 , which are encoded by two distinct genes of the Rel family .
0.9642 1.0000 1.0000 In most cases, the transcriptional factor NF-kappa B is a heterodimer consisting of two subunits, proteinp50 and p65 , which are encoded by two distinct genes of the Rel family .
0.9164 0.9992 1.0000 In most cases, the transcriptional factor proteinNF-kappa B is a heterodimer consisting of two subunits, p50 and p65 , which are encoded by two distinct genes of the Rel family .
In most cases, the transcriptional factor NF-kappa B is a heterodimer consisting of two subunits, p50 and p65 , which are encoded by two distinct genes of the DNARel family .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4083 10.9260 0.9999 p50 is translated as a precursor of protein105 kDa .
0.9762 1.0000 1.0000 proteinp50 is translated as a precursor of 105 kDa .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1006 20.6082 10.2467 The C-terminal domain of the precursor is rapidly degraded, forming the proteinmature p50 subunit consisted of the N-terminal region of the molecule.
2.0893 20.2047 0.9999 The C-terminal domain of the precursor is rapidly degraded, forming the mature p50 subunit consisted of the proteinN-terminal region of the molecule.
1.5043 10.4451 1.0000 The proteinC-terminal domain of the precursor is rapidly degraded, forming the mature p50 subunit consisted of the N-terminal region of the molecule.
0.9279 1.0000 0.9812 The C-terminal domain of the precursor is rapidly degraded, forming the mature proteinp50 subunit consisted of the N-terminal region of the molecule.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4463 10.6816 1.0000 The mechanism of generation of proteinp50 is not known.
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.8611 1.0000 1.0000 It has been suggested that the ubiquitin -proteasome system is involved in the process; however, the specific proteinenzymes involved and the mechanism of limited proteolysis , in which half of the molecule is spared, have been obscure.
0.8083 1.0000 0.9995 It has been suggested that the proteinubiquitin -proteasome system is involved in the process; however, the specific enzymes involved and the mechanism of limited proteolysis , in which half of the molecule is spared, have been obscure.
0.7616 1.0000 0.9984 It has been suggested that the ubiquitin protein-proteasome system is involved in the process; however, the specific enzymes involved and the mechanism of limited proteolysis , in which half of the molecule is spared, have been obscure.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6743 10.8004 0.9999 Palombella and colleagues (Palombella, V.J., Rando, O.J., Goldberg, A.L., and Maniatis, T.(1994) Cell 78, 773-785) have shown that ubiquitin is required for the processing in a cell-free system of a truncated, artificially constructed, protein60-kDa precursor .
0.8992 1.0000 1.0000 Palombella and colleagues (Palombella, V.J., Rando, O.J., Goldberg, A.L., and Maniatis, T.(1994) Cell 78, 773-785) have shown that proteinubiquitin is required for the processing in a cell-free system of a truncated, artificially constructed, 60-kDa precursor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.8492 1.0000 1.0000 They have also shown that proteinproteasome inhibitors block the processing both in vitro and in vivo.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4764 20.9941 10.3873 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of proteinubiquitin -protein ligase , is involved in the process.
2.4623 20.0418 0.9999 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact proteinp105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
2.3726 30.8848 10.5909 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the proteinubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
2.3077 20.8208 0.9958 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the proteinubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
2.2372 20.7912 1.0000 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the proteinp105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
1.7584 10.3008 1.0000 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of proteinp53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
1.0863 10.8893 0.9924 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of proteinubiquitin -protein ligase , is involved in the process.
0.9722 1.0000 1.0000 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , proteinE2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
0.9020 1.0000 1.0000 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of proteinubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
0.8391 1.0000 0.9999 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the proteinubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
3.0766 30.0626 0.9941 In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the proteinp105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin -proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately protein320-kDa species of ubiquitin -protein ligase , is involved in the process.
In this study, we demonstrate reconstitution of a cell-free processing system and demonstrate directly that: (a) the ubiquitin protein-proteasome system is involved in processing of the intact p105 precursor, (b) conjugation of ubiquitin to the precursor is an essential intermediate step in the processing, (c) the recently discovered novel species of the ubiquitin -carrier protein , E2-F1 , that is involved in the conjugation and degradation of p53 , is also required for the limited processing of the p105 precursor , and (d) a novel, approximately 320-kDa species of ubiquitin -protein ligase , is involved in the process.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5814 10.0021 0.9999 This novel enzyme is distinct from E6-AP , the p53 -conjugating ligase , and from E3 alpha , the protein"N-end rule" ligase .
0.8627 1.0000 1.0000 This novel enzyme is distinct from proteinE6-AP , the p53 -conjugating ligase , and from E3 alpha , the "N-end rule" ligase .
0.7865 0.9997 1.0000 This novel enzyme is distinct from E6-AP , the p53 -conjugating ligase , and from proteinE3 alpha , the "N-end rule" ligase .
0.7564 0.9970 0.9999 This novel enzyme is distinct from E6-AP , the proteinp53 -conjugating ligase , and from E3 alpha , the "N-end rule" ligase .
0.6062 1.0000 0.9985 This novel enzyme is distinct from E6-AP , the proteinp53 -conjugating ligase , and from E3 alpha , the "N-end rule" ligase .
This novel enzyme is distinct from E6-AP , the p53 -conjugating ligase , and from proteinE3 alpha , the "N-end rule" ligase .
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2.4152 20.3685 1.0000 Flutamide in the treatment of hirsutism : long-term clinical effects , endocrine changes , and proteinandrogen receptor behavior .
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2.6004 20.4772 1.0000 OBJECTIVE: To investigate the long-term effects of treatment with low doses of flutamide on clinical and hormonal parameters , as well as on the proteinandrogen receptor status, in hirsute women .
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2.4655 20.5127 1.0000 In addition, the concentration of proteinandrogen receptors in mononuclear leukocytes was measured, in both the follicular and luteal phases of the menstrual cycle , basally and after 4 months of flutamide treatment.
1.7231 10.8423 0.9999 In addition, the concentration of androgen receptors in cell_typemononuclear leukocytes was measured, in both the follicular and luteal phases of the menstrual cycle , basally and after 4 months of flutamide treatment.
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2.5414 20.6019 1.0000 RESULTS: Flutamide was well tolerated in all women , with the noticeable exception of one patient who presented increased proteinserum transaminase after 8 months of therapy .
RESULTS: Flutamide was well tolerated in all women , with the noticeable exception of one patient who presented increased serum transaminase after 8 months of proteintherapy .
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2.2863 20.1162 1.0000 A reduction of serum androgens was found, whereas no change was observed in either basal or proteinGnRH-stimulated gonadotropins or in the cortisol and 17 alpha-hydroxyprogesterone response to ACTH .
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2.4725 20.4024 1.0000 Before treatment, the number of proteinandrogen receptors was higher in the luteal than in the follicular phase .
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0.9156 0.9997 1.0000 proteinAndrogen receptor blockade might be potentiated by a reduction of serum androgens .
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1.5708 10.6652 1.0000 Flutamide affects proteinandrogen receptor behavior during the menstrual cycle .
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4.0301 20.5376 10.6752 Constitutive expression of HIV-1 tat protein in cell_linehuman Jurkat T cells using a BK virus vector .
3.8208 20.8760 10.8357 Constitutive expression of proteinHIV-1 tat protein in human Jurkat T cells using a BK virus vector .
Constitutive expression of HIV-1 tat protein in human cell_lineJurkat T cells using a BK virus vector .
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4.8709 10.6192 30.6793 The production and characterization of Jurkat cell lines that constitutively express functional proteinhuman immune deficiency virus type 1 ( HIV-1 ) tat protein , using a BK virus plasmid expression vector and HIV-1 tat cDNA , is described.
1.9300 10.1174 10.7562 The production and characterization of cell_lineJurkat cell lines that constitutively express functional human immune deficiency virus type 1 ( HIV-1 ) tat protein , using a BK virus plasmid expression vector and HIV-1 tat cDNA , is described.
1.3510 20.3144 0.9997 The production and characterization of Jurkat cell lines that constitutively express functional human immune deficiency virus type 1 ( HIV-1 ) tat protein , using a BK virus plasmid expression vector and DNAHIV-1 tat cDNA , is described.
4.3434 40.6071 20.9804 The production and characterization of Jurkat cell lines that constitutively express functional human immune deficiency virus type 1 ( HIV-1 ) tat protein , using a DNABK virus plasmid expression vector and HIV-1 tat cDNA , is described.
The production and characterization of Jurkat cell lines that constitutively express functional human immune deficiency virus type 1 ( HIV-1 ) proteintat protein , using a BK virus plasmid expression vector and HIV-1 tat cDNA , is described.
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4.2286 20.1666 10.6024 An increased growth rate of these Jurkat-tat cell lines as compared with cell_linecontrol cell lines was observed.
3.6277 20.2852 10.6007 An increased growth rate of these cell_lineJurkat-tat cell lines as compared with control cell lines was observed.
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3.3796 20.8964 10.2864 A PEBP2 alpha/AML-1-related factor increases osteocalcin promoter activity through its binding to an DNAosteoblast-specific cis-acting element .
3.0206 10.9282 10.8172 A proteinPEBP2 alpha/AML-1-related factor increases osteocalcin promoter activity through its binding to an osteoblast-specific cis-acting element .
1.4130 10.9233 0.9998 A PEBP2 alpha/AML-1-related factor increases DNAosteocalcin promoter activity through its binding to an osteoblast-specific cis-acting element .
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4.2620 20.5671 10.9465 To identify osteoblast-specific cis-acting elements and trans-acting factors , we initiated an analysis of the promoter of a DNAmouse osteocalcin gene , an osteoblast-specific gene .
3.3962 20.4548 10.6319 To identify DNAosteoblast-specific cis-acting elements and trans-acting factors , we initiated an analysis of the promoter of a mouse osteocalcin gene , an osteoblast-specific gene .
2.0689 20.4267 0.9997 To identify osteoblast-specific cis-acting elements and trans-acting factors , we initiated an analysis of the promoter of a mouse osteocalcin gene , an DNAosteoblast-specific gene .
1.4521 10.0991 0.9998 To identify osteoblast-specific cis-acting elements and proteintrans-acting factors , we initiated an analysis of the promoter of a mouse osteocalcin gene , an osteoblast-specific gene .
0.7948 0.9999 1.0000 To identify osteoblast-specific cis-acting elements and trans-acting factors , we initiated an analysis of the DNApromoter of a mouse osteocalcin gene , an osteoblast-specific gene .
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2.2638 10.5838 10.5145 In this promoter, we identified two DNAosteoblast-specific cis-acting elements (Ducy, P.and Karsenty, G.(1995) Mol.Cell.Biol.15, 1858-1869).
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3.9284 20.5696 10.6478 The sequence of one of these elements , OSE2 , is identical to the DNA-binding site of the proteinPEBP2 alpha/AML-1 transcription factors , the mammalian homologues of the Drosophila Runt protein .
3.2999 20.9540 10.9868 The sequence of one of these elements , OSE2 , is identical to the DNA-binding site of the PEBP2 alpha/AML-1 transcription factors , the mammalian homologues of the proteinDrosophila Runt protein .
2.1256 20.0730 0.9998 The sequence of one of these elements , OSE2 , is identical to the DNADNA-binding site of the PEBP2 alpha/AML-1 transcription factors , the mammalian homologues of the Drosophila Runt protein .
1.7236 10.6167 1.0000 The sequence of one of these elements , DNAOSE2 , is identical to the DNA-binding site of the PEBP2 alpha/AML-1 transcription factors , the mammalian homologues of the Drosophila Runt protein .
2.1702 20.0331 0.9983 The sequence of one of these elements , OSE2 , is identical to the DNA-binding site of the proteinPEBP2 alpha/AML-1 transcription factors , the mammalian homologues of the Drosophila Runt protein .
0.7903 0.9914 0.9999 The sequence of one of these elements , OSE2 , is identical to the DNA-binding site of the PEBP2 alpha/AML-1 proteintranscription factors , the mammalian homologues of the Drosophila Runt protein .
The sequence of one of these DNAelements , OSE2 , is identical to the DNA-binding site of the PEBP2 alpha/AML-1 transcription factors , the mammalian homologues of the Drosophila Runt protein .
The sequence of one of these elements , OSE2 , is identical to the DNA-binding site of the PEBP2 alpha/AML-1 transcription factors , the proteinmammalian homologues of the Drosophila Runt protein .
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2.4183 20.5543 1.0000 Here we show, using nuclear extracts , proteinrecombinant protein , and a specific antiserum against AML-1 proteins in DNA-binding assays , that one member of this family, AML-1B , binds specifically to OSE2 and is immunologically related to OSF2 , the factor present in osteoblast nuclear extracts that binds to OSE2 .
2.3972 20.3758 1.0000 Here we show, using nuclear extracts , recombinant protein , and a specific antiserum against proteinAML-1 proteins in DNA-binding assays , that one member of this family, AML-1B , binds specifically to OSE2 and is immunologically related to OSF2 , the factor present in osteoblast nuclear extracts that binds to OSE2 .
1.8468 10.1493 1.0000 Here we show, using nuclear extracts , recombinant protein , and a specific antiserum against AML-1 proteins in DNA-binding assays , that one member of this family, AML-1B , binds specifically to OSE2 and is immunologically related to proteinOSF2 , the factor present in osteoblast nuclear extracts that binds to OSE2 .
1.7979 10.2512 1.0000 Here we show, using nuclear extracts , recombinant protein , and a specific antiserum against AML-1 proteins in DNA-binding assays , that one member of this family, AML-1B , binds specifically to DNAOSE2 and is immunologically related to OSF2 , the factor present in osteoblast nuclear extracts that binds to OSE2 .
1.7131 10.2210 1.0000 Here we show, using nuclear extracts , recombinant protein , and a specific antiserum against AML-1 proteins in DNA-binding assays , that one member of this family, AML-1B , binds specifically to OSE2 and is immunologically related to OSF2 , the factor present in osteoblast nuclear extracts that binds to DNAOSE2 .
0.9594 1.0000 1.0000 Here we show, using nuclear extracts , recombinant protein , and a specific antiserum against AML-1 proteins in DNA-binding assays , that one member of this family, proteinAML-1B , binds specifically to OSE2 and is immunologically related to OSF2 , the factor present in osteoblast nuclear extracts that binds to OSE2 .
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1.6013 10.3213 1.0000 By DNA cotransfection experiments , we also demonstrate that AML-1B can increase the activity of a short osteocalcin promoter through its binding to DNAOSE2 .
1.5748 10.8438 1.0000 By DNA cotransfection experiments , we also demonstrate that AML-1B can increase the activity of a short DNAosteocalcin promoter through its binding to OSE2 .
0.8596 1.0000 1.0000 By DNA cotransfection experiments , we also demonstrate that proteinAML-1B can increase the activity of a short osteocalcin promoter through its binding to OSE2 .
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5.4269 30.5717 10.6756 Lastly, the different mobilities of osteoblast nuclear extract-DNA complexes compared with proteinT-cell nuclear extract-DNA complexes , along with the inability of OSF2 to be upregulated by retinoic acid , unlike the other PEBP2 alpha factors , suggest that OSF2 is a new member of this family of transcription factors .
4.6723 20.7820 10.4023 Lastly, the different mobilities of proteinosteoblast nuclear extract-DNA complexes compared with T-cell nuclear extract-DNA complexes , along with the inability of OSF2 to be upregulated by retinoic acid , unlike the other PEBP2 alpha factors , suggest that OSF2 is a new member of this family of transcription factors .
2.9608 20.5007 10.6260 Lastly, the different mobilities of osteoblast nuclear extract-DNA complexes compared with T-cell nuclear extract-DNA complexes , along with the inability of OSF2 to be upregulated by retinoic acid , unlike the other proteinPEBP2 alpha factors , suggest that OSF2 is a new member of this family of transcription factors .
1.4989 10.3113 1.0000 Lastly, the different mobilities of osteoblast nuclear extract-DNA complexes compared with T-cell nuclear extract-DNA complexes , along with the inability of proteinOSF2 to be upregulated by retinoic acid , unlike the other PEBP2 alpha factors , suggest that OSF2 is a new member of this family of transcription factors .
1.4643 10.8055 0.9999 Lastly, the different mobilities of osteoblast nuclear extract-DNA complexes compared with T-cell nuclear extract-DNA complexes , along with the inability of OSF2 to be upregulated by retinoic acid , unlike the other PEBP2 alpha factors , suggest that OSF2 is a new member of this family of proteintranscription factors .
0.8412 1.0000 1.0000 Lastly, the different mobilities of osteoblast nuclear extract-DNA complexes compared with T-cell nuclear extract-DNA complexes , along with the inability of OSF2 to be upregulated by retinoic acid , unlike the other PEBP2 alpha factors , suggest that proteinOSF2 is a new member of this family of transcription factors .
2.0118 20.6365 0.9969 Lastly, the different mobilities of osteoblast nuclear extract-DNA complexes compared with T-cell nuclear extract-DNA complexes , along with the inability of OSF2 to be upregulated by retinoic acid , unlike the other proteinPEBP2 alpha factors , suggest that OSF2 is a new member of this family of transcription factors .
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3.6463 20.9161 10.6568 Thus, this study demonstrates that AML-1B can increase gene expression of an osteoblast-specific gene through its binding to an DNAosteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the PEBP2 alpha/AML-1 family of transcription factors .
2.4788 30.5019 0.9757 Thus, this study demonstrates that AML-1B can increase gene expression of an osteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the proteinPEBP2 alpha/AML-1 family of transcription factors .
2.0717 20.7693 1.0000 Thus, this study demonstrates that AML-1B can increase gene expression of an DNAosteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the PEBP2 alpha/AML-1 family of transcription factors .
1.4903 10.3728 1.0000 Thus, this study demonstrates that proteinAML-1B can increase gene expression of an osteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the PEBP2 alpha/AML-1 family of transcription factors .
0.8295 0.9921 0.9998 Thus, this study demonstrates that AML-1B can increase gene expression of an osteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the PEBP2 alpha/AML-1 family of proteintranscription factors .
0.7903 1.0000 1.0000 Thus, this study demonstrates that AML-1B can increase gene expression of an osteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that proteinOSF2 is a member of the PEBP2 alpha/AML-1 family of transcription factors .
4.1788 30.1657 10.9547 Thus, this study demonstrates that AML-1B can increase gene expression of an osteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the proteinPEBP2 alpha/AML-1 family of transcription factors .
0.7219 1.0000 0.9988 Thus, this study demonstrates that AML-1B can increase gene expression of an osteoblast-specific gene through its binding to an osteoblast-specific cis-acting element and presents evidence that OSF2 is a member of the proteinPEBP2 alpha/AML-1 family of transcription factors .
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4.5217 30.1780 10.8938 Initiation binding repressor , a factor that binds to the transcription initiation site of the DNAhistone h5 gene , is a glycosylated member of a family of cell growth regulators [corrected] [published erratum appears in Mol Cell Biol 1996 Feb;16(2):735]
3.5630 20.9018 10.9970 Initiation binding repressor , a factor that binds to the DNAtranscription initiation site of the histone h5 gene , is a glycosylated member of a family of cell growth regulators [corrected] [published erratum appears in Mol Cell Biol 1996 Feb;16(2):735]
2.2361 20.3492 10.1001 Initiation binding repressor , a factor that binds to the transcription initiation site of the histone h5 gene , is a glycosylated member of a family of proteincell growth regulators [corrected] [published erratum appears in Mol Cell Biol 1996 Feb;16(2):735]
1.5836 0.9989 10.6373 proteinInitiation binding repressor , a factor that binds to the transcription initiation site of the histone h5 gene , is a glycosylated member of a family of cell growth regulators [corrected] [published erratum appears in Mol Cell Biol 1996 Feb;16(2):735]
Initiation binding repressor , a factor that binds to the transcription initiation site of the histone h5 gene , is a proteinglycosylated member of a family of cell growth regulators [corrected] [published erratum appears in Mol Cell Biol 1996 Feb;16(2):735]
Initiation binding repressor , a factor that binds to the transcription initiation site of the proteinhistone h5 gene , is a glycosylated member of a family of cell growth regulators [corrected] [published erratum appears in Mol Cell Biol 1996 Feb;16(2):735]
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3.7329 20.4637 10.7173 Initiation binding repressor [corrected] ( IBR ) is a chicken erythrocyte factor (apparent molecular mass, 70 to 73 kDa) that binds to the sequences spanning the transcription initiation site of the DNAhistone h5 gene , repressing its transcription .
3.5001 20.8177 10.7436 Initiation binding repressor [corrected] ( IBR ) is a proteinchicken erythrocyte factor (apparent molecular mass, 70 to 73 kDa) that binds to the sequences spanning the transcription initiation site of the histone h5 gene , repressing its transcription .
3.4472 20.7710 10.7553 Initiation binding repressor [corrected] ( IBR ) is a chicken erythrocyte factor (apparent molecular mass, 70 to 73 kDa) that binds to the sequences spanning the DNAtranscription initiation site of the histone h5 gene , repressing its transcription .
1.5992 0.9991 10.7189 proteinInitiation binding repressor [corrected] ( IBR ) is a chicken erythrocyte factor (apparent molecular mass, 70 to 73 kDa) that binds to the sequences spanning the transcription initiation site of the histone h5 gene , repressing its transcription .
0.9514 1.0000 1.0000 Initiation binding repressor [corrected] ( proteinIBR ) is a chicken erythrocyte factor (apparent molecular mass, 70 to 73 kDa) that binds to the sequences spanning the transcription initiation site of the histone h5 gene , repressing its transcription .
Initiation binding repressor [corrected] ( IBR ) is a chicken erythrocyte factor (apparent molecular mass, 70 to 73 kDa) that binds to the sequences spanning the transcription initiation site of the proteinhistone h5 gene , repressing its transcription .
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2.0361 20.3962 0.9998 A variety of other cells, including transformed erythroid precursors , do not have IBR but a factor referred to as IBF (68 to 70 kDa) that recognizes the same proteinIBR sites.
1.6678 10.3739 0.9999 A variety of other cells, including transformed erythroid precursors , do not have IBR but a factor referred to as proteinIBF (68 to 70 kDa) that recognizes the same IBR sites.
1.6635 10.0502 1.0000 A variety of other cells, including transformed erythroid precursors , do not have proteinIBR but a factor referred to as IBF (68 to 70 kDa) that recognizes the same IBR sites.
3.7755 20.8764 10.7418 A variety of other cells, including cell_linetransformed erythroid precursors , do not have IBR but a factor referred to as IBF (68 to 70 kDa) that recognizes the same IBR sites.
A variety of other cells, including cell_typetransformed erythroid precursors , do not have IBR but a factor referred to as IBF (68 to 70 kDa) that recognizes the same IBR sites.
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2.1418 20.1512 1.0000 We have cloned the DNAIBR cDNA and studied the relationship of IBR and IBF .
2.0424 20.0418 0.9919 We have cloned the proteinIBR cDNA and studied the relationship of IBR and IBF .
1.4623 10.5998 1.0000 We have cloned the IBR cDNA and studied the relationship of proteinIBR and IBF .
0.8416 1.0000 1.0000 We have cloned the IBR cDNA and studied the relationship of IBR and proteinIBF .
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4.6877 20.3444 10.8298 IBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the invertebrate transcription factors P3A2 and proteinerected wing gene product ( EWG ).
3.6373 20.6153 10.3064 IBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported proteinhuman NRF-1/alpha-Pal factor and highly related to the invertebrate transcription factors P3A2 and erected wing gene product ( EWG ).
3.6119 20.9199 10.4910 IBR is a protein503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the invertebrate transcription factors P3A2 and erected wing gene product ( EWG ).
0.9689 1.0000 1.0000 proteinIBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the invertebrate transcription factors P3A2 and erected wing gene product ( EWG ).
0.9668 1.0000 1.0000 IBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the invertebrate transcription factors P3A2 and erected wing gene product ( proteinEWG ).
0.9508 0.9997 1.0000 IBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the invertebrate transcription factors proteinP3A2 and erected wing gene product ( EWG ).
4.0683 20.9335 10.8906 IBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the proteininvertebrate transcription factors P3A2 and erected wing gene product ( EWG ).
IBR is a 503-amino-acid-long acidic protein which is 99.0% identical to the recently reported human NRF-1/alpha-Pal factor and highly related to the invertebrate proteintranscription factors P3A2 and erected wing gene product ( EWG ).
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1.7420 10.4233 1.0000 We present evidence that proteinIBR and IBF are most likely identical proteins, differing in their degree of glycosylation .
0.9729 1.0000 1.0000 We present evidence that IBR and proteinIBF are most likely identical proteins, differing in their degree of glycosylation .
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1.5723 10.4187 1.0000 We have analyzed several molecular aspects of proteinIBR/F and shown that the factor associates as stable homodimers and that the dimer is the relevant DNA-binding species .
0.8877 1.0000 1.0000 We have analyzed several molecular aspects of IBR/F and shown that the factor associates as stable homodimers and that the proteindimer is the relevant DNA-binding species .
0.8723 1.0000 1.0000 We have analyzed several molecular aspects of IBR/F and shown that the factor associates as stable proteinhomodimers and that the dimer is the relevant DNA-binding species .
1.5102 10.9928 0.9999 We have analyzed several molecular aspects of IBR/F and shown that the factor associates as stable homodimers and that the dimer is the relevant proteinDNA-binding species .
We have analyzed several molecular aspects of IBR/F and shown that the factor associates as stable homodimers and that the dimer is the proteinrelevant DNA-binding species .
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4.1678 20.9155 10.9844 The evolutionarily conserved N-terminal half of IBR/F harbors the DNA-binding/dimerization domain (outer limits, 127 to 283), one or several casein kinase II sites (37 to 67), and a proteinbipartite nuclear localization signal (89 to 106) which appears to be necessary for nuclear targeting .
1.3592 10.8461 0.9998 The evolutionarily conserved N-terminal half of IBR/F harbors the proteinDNA-binding/dimerization domain (outer limits, 127 to 283), one or several casein kinase II sites (37 to 67), and a bipartite nuclear localization signal (89 to 106) which appears to be necessary for nuclear targeting .
0.8759 0.9999 1.0000 The evolutionarily conserved N-terminal half of proteinIBR/F harbors the DNA-binding/dimerization domain (outer limits, 127 to 283), one or several casein kinase II sites (37 to 67), and a bipartite nuclear localization signal (89 to 106) which appears to be necessary for nuclear targeting .
0.7753 0.9942 0.9999 The evolutionarily conserved proteinN-terminal half of IBR/F harbors the DNA-binding/dimerization domain (outer limits, 127 to 283), one or several casein kinase II sites (37 to 67), and a bipartite nuclear localization signal (89 to 106) which appears to be necessary for nuclear targeting .
1.2531 20.7883 10.4576 The evolutionarily conserved N-terminal half of IBR/F harbors the DNA-binding/dimerization domain (outer limits, 127 to 283), one or several proteincasein kinase II sites (37 to 67), and a bipartite nuclear localization signal (89 to 106) which appears to be necessary for nuclear targeting .
The evolutionarily conserved N-terminal half of IBR/F harbors the DNA-binding/dimerization domain (outer limits, 127 to 283), one or several proteincasein kinase II sites (37 to 67), and a bipartite nuclear localization signal (89 to 106) which appears to be necessary for nuclear targeting .
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1.9779 20.4571 0.9998 Binding site selection revealed that the alternating RCGCRYGCGY consensus constitutes high-affinity IBR/F binding sites and that the DNAdirect-repeat palindrome TGCGCATGCGCA is the optimal site .
1.3476 10.4932 0.9995 Binding site selection revealed that the alternating RCGCRYGCGY consensus constitutes high-affinity IBR/F binding sites and that the direct-repeat palindrome TGCGCATGCGCA is the DNAoptimal site .
0.8963 1.0000 0.9979 Binding site selection revealed that the alternating RCGCRYGCGY consensus constitutes high-affinity proteinIBR/F binding sites and that the direct-repeat palindrome TGCGCATGCGCA is the optimal site .
4.1256 20.4418 10.5965 Binding site selection revealed that the alternating RCGCRYGCGY consensus constitutes DNAhigh-affinity IBR/F binding sites and that the direct-repeat palindrome TGCGCATGCGCA is the optimal site .
Binding site selection revealed that the proteinalternating RCGCRYGCGY consensus constitutes high-affinity IBR/F binding sites and that the direct-repeat palindrome TGCGCATGCGCA is the optimal site .
Binding site selection revealed that the alternating RCGCRYGCGY consensus constitutes high-affinity DNAIBR/F binding sites and that the direct-repeat palindrome TGCGCATGCGCA is the optimal site .
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0.9116 1.0000 1.0000 A survey of genes potentially regulated by this family of factors primarily revealed DNAgenes involved in growth-related metabolism .
0.6312 0.9998 1.0000 A survey of DNAgenes potentially regulated by this family of factors primarily revealed genes involved in growth-related metabolism .
A survey of genes potentially regulated by this family of proteinfactors primarily revealed genes involved in growth-related metabolism .
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3.8477 20.8034 10.4882 Triggering of the human interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between proteininterferon regulatory factor-1 , NF kappa B , and Sp1 transcription factors .
2.1251 10.3902 10.4674 Triggering of the human interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , proteinNF kappa B , and Sp1 transcription factors .
1.6092 20.3449 0.9998 Triggering of the human interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B , and Sp1 proteintranscription factors .
1.5494 10.5743 0.9999 Triggering of the human interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B , and proteinSp1 transcription factors .
3.3059 20.6272 10.6014 Triggering of the DNAhuman interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B , and Sp1 transcription factors .
2.7060 10.8142 10.9371 Triggering of the human interleukin-6 gene by interferon-gamma and proteintumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B , and Sp1 transcription factors .
1.3977 10.2376 0.9998 Triggering of the human interleukin-6 gene by interferon-gamma and tumor necrosis factor-alpha in cell_typemonocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B , and Sp1 transcription factors .
0.9164 1.0000 1.0000 Triggering of the human interleukin-6 gene by proteininterferon-gamma and tumor necrosis factor-alpha in monocytic cells involves cooperation between interferon regulatory factor-1 , NF kappa B , and Sp1 transcription factors .
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3.9651 20.7867 10.9242 We investigated the molecular basis of the synergistic induction by interferon-gamma ( IFN-gamma )/ tumor necrosis factor-alpha ( TNF-alpha ) of DNAhuman interleukin-6 (IL-6) gene in THP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
2.8813 10.5995 10.6271 We investigated the molecular basis of the synergistic induction by interferon-gamma ( IFN-gamma )/ proteintumor necrosis factor-alpha ( TNF-alpha ) of human interleukin-6 (IL-6) gene in THP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
0.9754 1.0000 1.0000 We investigated the molecular basis of the synergistic induction by interferon-gamma ( proteinIFN-gamma )/ tumor necrosis factor-alpha ( TNF-alpha ) of human interleukin-6 (IL-6) gene in THP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
0.9703 1.0000 1.0000 We investigated the molecular basis of the synergistic induction by interferon-gamma ( IFN-gamma )/ tumor necrosis factor-alpha ( proteinTNF-alpha ) of human interleukin-6 (IL-6) gene in THP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
0.8708 1.0000 1.0000 We investigated the molecular basis of the synergistic induction by proteininterferon-gamma ( IFN-gamma )/ tumor necrosis factor-alpha ( TNF-alpha ) of human interleukin-6 (IL-6) gene in THP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
1.7589 10.8268 10.5871 We investigated the molecular basis of the synergistic induction by interferon-gamma ( IFN-gamma )/ tumor necrosis factor-alpha ( TNF-alpha ) of human interleukin-6 (IL-6) gene in cell_lineTHP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
0.6737 1.0000 0.9994 We investigated the molecular basis of the synergistic induction by interferon-gamma ( IFN-gamma )/ tumor necrosis factor-alpha ( TNF-alpha ) of human interleukin-6 (IL-6) gene in THP-1 cell_typemonocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
We investigated the molecular basis of the synergistic induction by interferon-gamma ( IFN-gamma )/ tumor necrosis factor-alpha ( TNF-alpha ) of human interleukin-6 (IL-6) gene in cell_typeTHP-1 monocytic cells , and compared it with the basis of this induction by lipopolysaccharide ( LPS ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3539 20.8270 1.0000 Functional studies with DNAIL-6 promoter demonstrated that three regions are the targets of the IFN-gamma and/or TNF-alpha action, whereas only one of these regions seemed to be implicated in LPS activation .
0.9157 1.0000 1.0000 Functional studies with IL-6 promoter demonstrated that three regions are the targets of the IFN-gamma and/or proteinTNF-alpha action, whereas only one of these regions seemed to be implicated in LPS activation .
0.8845 1.0000 1.0000 Functional studies with IL-6 promoter demonstrated that three regions are the targets of the proteinIFN-gamma and/or TNF-alpha action, whereas only one of these regions seemed to be implicated in LPS activation .
2.2726 20.9912 0.9935 Functional studies with proteinIL-6 promoter demonstrated that three regions are the targets of the IFN-gamma and/or TNF-alpha action, whereas only one of these regions seemed to be implicated in LPS activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6344 10.1561 1.0000 The three regions concerned are: 1) a region between -73 and -36, which is the minimal element inducible by LPS or proteinTNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and TNF-alpha negatively; and 3) a distal element upstream of -224, which was inducible by IFN-gamma alone.
1.5526 10.4065 1.0000 The three regions concerned are: 1) a region between -73 and -36, which is the minimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and TNF-alpha negatively; and 3) a distal element upstream of -224, which was inducible by proteinIFN-gamma alone.
0.9300 1.0000 1.0000 The three regions concerned are: 1) a region between -73 and -36, which is the minimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and proteinTNF-alpha negatively; and 3) a distal element upstream of -224, which was inducible by IFN-gamma alone.
0.8823 1.0000 1.0000 The three regions concerned are: 1) a region between -73 and -36, which is the minimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to proteinIFN-gamma and TNF-alpha negatively; and 3) a distal element upstream of -224, which was inducible by IFN-gamma alone.
1.1197 10.9331 0.9999 The three regions concerned are: 1) a region between DNA-73 and -36, which is the minimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and TNF-alpha negatively; and 3) a distal element upstream of -224, which was inducible by IFN-gamma alone.
0.7396 0.9999 1.0000 The three regions concerned are: 1) a region between -73 and -36, which is the minimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and TNF-alpha negatively; and 3) a distal element upstream of DNA-224, which was inducible by IFN-gamma alone.
The three regions concerned are: 1) a region between -73 and -36, which is the DNAminimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and TNF-alpha negatively; and 3) a distal element upstream of -224, which was inducible by IFN-gamma alone.
The three regions concerned are: 1) a region between -73 and -36, which is the minimal element inducible by LPS or TNF-alpha ; 2) an element located between -181 and -73, which appeared to regulate the response to IFN-gamma and TNF-alpha negatively; and 3) a DNAdistal element upstream of -224, which was inducible by IFN-gamma alone.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4073 20.1958 10.5572 LPS signaling was found to involve proteinNF kappa B activation by the p50/p65 heterodimers .
1.3642 10.8479 0.9999 LPS signaling was found to involve NF kappa B activation by the proteinp50/p65 heterodimers .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5588 20.6994 10.7371 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the DNAretinoblastoma control element present in the IL-6 promoter .
2.7592 10.9276 10.6051 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and proteinNF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
2.0969 20.2017 0.9999 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the DNAIL-6 promoter .
2.0544 20.1127 1.0000 Synergistic induction of the DNAIL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
2.0105 20.4085 0.9924 Synergistic induction of the proteinIL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
1.4300 10.9693 0.9998 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in cell_typemonocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
0.9767 1.0000 1.0000 Synergistic induction of the IL-6 gene by IFN-gamma and proteinTNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
0.9537 1.0000 1.0000 Synergistic induction of the IL-6 gene by proteinIFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
0.8618 0.9999 1.0000 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the proteinIRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
0.8408 0.9992 0.9642 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B proteinp65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
1.9623 20.5697 0.9847 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the proteinIL-6 promoter .
0.8666 0.9794 0.9998 Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and NF kappa B proteinp65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
Synergistic induction of the IL-6 gene by IFN-gamma and TNF-alpha , in monocytic cells , involved cooperation between the IRF-1 and proteinNF kappa B p65 homodimers with concomitant removal of the negative effect of the retinoblastoma control element present in the IL-6 promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1694 20.1809 10.0860 This removal occurred by activation of the proteinconstitutive Sp1 factor , whose increased binding activity and phosphorylation were mediated by IFN-gamma .
1.4619 10.5958 1.0000 This removal occurred by activation of the constitutive Sp1 factor , whose increased binding activity and phosphorylation were mediated by proteinIFN-gamma .
0.8809 1.0000 0.9834 This removal occurred by activation of the constitutive proteinSp1 factor , whose increased binding activity and phosphorylation were mediated by IFN-gamma .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6165 10.5602 1.0000 Mutation of Jak3 in a patient with SCID : essential role of proteinJak3 in lymphoid development .
1.5852 10.9511 1.0000 Mutation of proteinJak3 in a patient with SCID : essential role of Jak3 in lymphoid development .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5064 10.9565 1.0000 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and proteinIL-15 .
0.9712 1.0000 1.0000 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( proteinIL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
0.9513 1.0000 1.0000 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , proteinIL-7 , IL-9 , and IL-15 .
0.9503 1.0000 1.0000 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), proteinIL-4 , IL-7 , IL-9 , and IL-15 .
0.9405 1.0000 1.0000 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , proteinIL-9 , and IL-15 .
0.8950 1.0000 1.0000 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of proteininterleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
0.7860 1.0000 0.9217 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common cytokine receptor gamma chain ( proteingamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
6.1389 20.4570 20.7346 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the DNAcommon cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
2.6346 40.6945 10.4216 Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the proteincommon cytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common proteincytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
Males with X-linked severe combined immunodeficiency ( XSCID ) have defects in the common DNAcytokine receptor gamma chain ( gamma c ) gene that encodes a shared, essential component of the receptors of interleukin-2 ( IL-2 ), IL-4 , IL-7 , IL-9 , and IL-15 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2654 20.0620 1.0000 The Janus family tyrosine kinase Jak3 is the only signaling molecule known to be associated with gamma c , so it was hypothesized that defects in proteinJak3 might cause an XSCID -like phenotype .
2.1359 20.4090 0.9999 The Janus family tyrosine kinase Jak3 is the only signaling molecule known to be associated with proteingamma c , so it was hypothesized that defects in Jak3 might cause an XSCID -like phenotype .
1.6010 10.9002 0.9925 The proteinJanus family tyrosine kinase Jak3 is the only signaling molecule known to be associated with gamma c , so it was hypothesized that defects in Jak3 might cause an XSCID -like phenotype .
0.9771 0.9999 1.0000 The Janus family tyrosine kinase proteinJak3 is the only signaling molecule known to be associated with gamma c , so it was hypothesized that defects in Jak3 might cause an XSCID -like phenotype .
1.3152 10.1734 0.9997 The Janus family tyrosine kinase Jak3 is the only proteinsignaling molecule known to be associated with gamma c , so it was hypothesized that defects in Jak3 might cause an XSCID -like phenotype .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5262 10.2507 10.2276 An cell_lineEpstein-Barr virus ( EBV )-transformed cell line derived from her lymphocytes had normal gamma c expression but lacked Jak3 protein and had greatly diminished Jak3 messenger RNA .
2.4424 30.6626 10.9273 An Epstein-Barr virus ( EBV )-transformed cell line derived from her lymphocytes had normal gamma c expression but lacked Jak3 protein and had greatly diminished RNAJak3 messenger RNA .
1.6320 20.7928 1.0000 An Epstein-Barr virus ( EBV )-transformed cell line derived from her lymphocytes had normal gamma c expression but lacked proteinJak3 protein and had greatly diminished Jak3 messenger RNA .
1.1686 10.9495 0.9999 An Epstein-Barr virus ( EBV )-transformed cell line derived from her lymphocytes had normal proteingamma c expression but lacked Jak3 protein and had greatly diminished Jak3 messenger RNA .
1.1089 20.4258 0.9886 An Epstein-Barr virus ( EBV )-transformed cell line derived from her lymphocytes had normal gamma c expression but lacked proteinJak3 protein and had greatly diminished Jak3 messenger RNA .
0.7927 0.9999 0.9999 An Epstein-Barr virus ( EBV )-transformed cell line derived from her cell_typelymphocytes had normal gamma c expression but lacked Jak3 protein and had greatly diminished Jak3 messenger RNA .
An Epstein-Barr virus ( EBV )-transformed cell line derived from her lymphocytes had normal gamma c expression but lacked Jak3 protein and had greatly diminished proteinJak3 messenger RNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.4314 30.2045 10.7056 Sequencing revealed a different mutation on each allele: a single nucleotide insertion resulting in a frame shift and premature termination in the DNAJak3 JH4 domain and a nonsense mutation in the Jak3 JH2 domain .
3.6976 30.2136 10.9476 Sequencing revealed a different mutation on each allele: a single nucleotide insertion resulting in a frame shift and premature termination in the Jak3 JH4 domain and a nonsense mutation in the DNAJak3 JH2 domain .
3.5455 20.8213 10.5987 Sequencing revealed a different mutation on each allele: a DNAsingle nucleotide insertion resulting in a frame shift and premature termination in the Jak3 JH4 domain and a nonsense mutation in the Jak3 JH2 domain .
Sequencing revealed a different mutation on each allele: a single nucleotide insertion resulting in a frame shift and premature termination in the Jak3 JH4 domain and a nonsense mutation in the proteinJak3 JH2 domain .
Sequencing revealed a different mutation on each allele: a single nucleotide insertion resulting in a frame shift and premature termination in the proteinJak3 JH4 domain and a nonsense mutation in the Jak3 JH2 domain .
Sequencing revealed a different mutation on each allele: a single nucleotide insertion resulting in a frame shift and premature termination in the proteinJak3 JH4 domain and a nonsense mutation in the Jak3 JH2 domain .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.9598 30.0911 10.8405 The lack of Jak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of IL-4 to activate Stat6 in the cell_lineEBV -transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on Jak3 and that Jak3 is essential for lymphoid development and signaling.
2.4006 20.2791 1.0000 The lack of proteinJak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of IL-4 to activate Stat6 in the EBV -transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on Jak3 and that Jak3 is essential for lymphoid development and signaling.
2.3661 20.9761 0.9999 The lack of Jak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of IL-4 to activate Stat6 in the EBV -transformed cell line from the patient. These observations indicate that the functions of proteingamma c are dependent on Jak3 and that Jak3 is essential for lymphoid development and signaling.
1.7087 10.3122 1.0000 The lack of Jak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of proteinIL-4 to activate Stat6 in the EBV -transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on Jak3 and that Jak3 is essential for lymphoid development and signaling.
1.6784 10.6784 1.0000 The lack of Jak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of IL-4 to activate proteinStat6 in the EBV -transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on Jak3 and that Jak3 is essential for lymphoid development and signaling.
1.6134 10.7899 1.0000 The lack of Jak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of IL-4 to activate Stat6 in the EBV -transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on proteinJak3 and that Jak3 is essential for lymphoid development and signaling.
0.8820 1.0000 1.0000 The lack of Jak3 expression correlated with impaired B cell signaling , as demonstrated by the inability of IL-4 to activate Stat6 in the EBV -transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on Jak3 and that proteinJak3 is essential for lymphoid development and signaling.
Cls_Score Left_Reg_Score Right_Reg_Score Text
7.1908 40.1420 20.6059 Constitutive overexpression of the L-selectin gene in fresh leukemic cells of adult T-cell leukemia that can be transactivated by proteinhuman T-cell lymphotropic virus type 1 Tax .
2.7016 20.3588 10.0913 Constitutive overexpression of the L-selectin gene in fresh cell_typeleukemic cells of adult T-cell leukemia that can be transactivated by human T-cell lymphotropic virus type 1 Tax .
1.8549 20.9114 1.0000 Constitutive overexpression of the DNAL-selectin gene in fresh leukemic cells of adult T-cell leukemia that can be transactivated by human T-cell lymphotropic virus type 1 Tax .
Constitutive overexpression of the proteinL-selectin gene in fresh leukemic cells of adult T-cell leukemia that can be transactivated by human T-cell lymphotropic virus type 1 Tax .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9644 1.0000 1.0000 proteinL-selectin is an adhesion molecule of the selectin family that mediates the initial step of leukocyte adhesion to vascular endothelium .
2.2366 20.2749 1.0000 L-selectin is an proteinadhesion molecule of the selectin family that mediates the initial step of leukocyte adhesion to vascular endothelium .
2.2103 20.0911 1.0000 L-selectin is an adhesion molecule of the proteinselectin family that mediates the initial step of leukocyte adhesion to vascular endothelium .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3328 20.4157 0.9960 Upon cellular activation , expression of the proteinL-selectin gene is downregulated at both the protein and mRNA levels .
2.2947 20.4238 1.0000 Upon cellular activation , expression of the DNAL-selectin gene is downregulated at both the protein and mRNA levels .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.2065 20.9198 30.9060 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of L-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the L-selectin promoter to proteinhuman T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
2.2982 20.2936 1.0000 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of RNAL-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the L-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
2.2585 10.5868 10.6430 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of L-selectin mRNA in fresh cell_typeleukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the L-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
1.9608 20.5985 0.9997 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of L-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the DNAL-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
1.9458 20.6989 0.9910 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of proteinL-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the L-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
1.3509 20.4339 0.9625 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of L-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the proteinL-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
1.3026 10.0761 0.9998 To understand the mechanism of cell_typeleukemic cell infiltration into organs , we studied the expression and regulation of L-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the L-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a viral transcriptional transactivator .
0.5622 0.9957 0.9990 To understand the mechanism of leukemic cell infiltration into organs , we studied the expression and regulation of L-selectin mRNA in fresh leukemic cells of adult T-cell leukemia ( ATL ) patients and investigated the response of the L-selectin promoter to human T-cell lymphotropic virus type 1 ( HTLV-1 ) Tax , which is a proteinviral transcriptional transactivator .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6662 10.1234 1.0000 Flow cytometry showed that proteinL-selectin was expressed on fresh ATL cells along with other activation antigens .
1.3650 10.9843 0.9999 Flow cytometry showed that L-selectin was expressed on fresh ATL cells along with other proteinactivation antigens .
Flow cytometry showed that L-selectin was expressed on fresh cell_lineATL cells along with other activation antigens .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6596 10.9462 1.0000 Northern blot analysis showed that ATL cells overexpressed that RNAL-selectin mRNA and that the level was aberrantly upregulated after PMA stimulation .
1.5838 10.9582 0.9999 Northern blot analysis showed that cell_lineATL cells overexpressed that L-selectin mRNA and that the level was aberrantly upregulated after PMA stimulation .
1.4236 10.8723 0.9939 Northern blot analysis showed that ATL cells overexpressed that proteinL-selectin mRNA and that the level was aberrantly upregulated after PMA stimulation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4953 20.5486 1.0000 Studies using in situ hybridization showed expression of the RNAL-selectin mRNA in the infiltrating leukemic cells in the liver of two ATL patients .
2.0134 20.6820 0.9885 Studies using in situ hybridization showed expression of the proteinL-selectin mRNA in the infiltrating leukemic cells in the liver of two ATL patients .
1.0483 1.0000 10.3702 Studies using in situ hybridization showed expression of the L-selectin mRNA in the infiltrating cell_typeleukemic cells in the liver of two ATL patients .
4.5376 20.2887 10.7338 Studies using in situ hybridization showed expression of the L-selectin mRNA in the cell_typeinfiltrating leukemic cells in the liver of two ATL patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8304 20.0701 10.8579 Intravenous injection of a cell_linerat T-cell line that overexpresses L-selectin showed increased organ infiltration .
1.6117 10.5333 1.0000 Intravenous injection of a rat T-cell line that overexpresses proteinL-selectin showed increased organ infiltration .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7328 10.5816 1.0000 The induction of proteinTax expression in JPX9 cells resulted in about a twofold increase in the mRNA expression levels compared with the basal level .
1.6295 10.9699 0.9999 The induction of Tax expression in cell_lineJPX9 cells resulted in about a twofold increase in the mRNA expression levels compared with the basal level .
1.5137 10.0010 1.0000 The induction of Tax expression in JPX9 cells resulted in about a twofold increase in the RNAmRNA expression levels compared with the basal level .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1957 20.6145 0.9999 Chloramphenicol acetyltransferase ( CAT ) assay after transient cotransfection showed about a fivefold transactivation of the DNAL-selectin promoter by Tax .
0.9709 1.0000 1.0000 Chloramphenicol acetyltransferase ( proteinCAT ) assay after transient cotransfection showed about a fivefold transactivation of the L-selectin promoter by Tax .
0.8824 0.9995 1.0000 proteinChloramphenicol acetyltransferase ( CAT ) assay after transient cotransfection showed about a fivefold transactivation of the L-selectin promoter by Tax .
0.8584 1.0000 1.0000 Chloramphenicol acetyltransferase ( CAT ) assay after transient cotransfection showed about a fivefold transactivation of the L-selectin promoter by proteinTax .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9576 1.0000 1.0000 The serum level of the shed form of proteinL-selectin was significantly increased in ATL patients (mean +/- SD, 4,215.4 +/- 4,111 ng/mL) compared with those of asymptomatic carriers and healthy blood donors (mean +/- SD, 1,148.0 +/- 269.0 ng/mL and 991.9 +/- 224 ng/mL, respectively).
2.3241 20.6272 1.0000 The serum level of the proteinshed form of L-selectin was significantly increased in ATL patients (mean +/- SD, 4,215.4 +/- 4,111 ng/mL) compared with those of asymptomatic carriers and healthy blood donors (mean +/- SD, 1,148.0 +/- 269.0 ng/mL and 991.9 +/- 224 ng/mL, respectively).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1607 20.0722 0.9943 These results indicated that ATL cells constitutively overexpress the proteinL-selectin gene that can be transactivated by HTLV-1 Tax .
1.5382 10.8679 0.9999 These results indicated that cell_lineATL cells constitutively overexpress the L-selectin gene that can be transactivated by HTLV-1 Tax .
1.4835 10.9032 1.0000 These results indicated that ATL cells constitutively overexpress the DNAL-selectin gene that can be transactivated by HTLV-1 Tax .
1.4919 10.8181 0.9999 These results indicated that ATL cells constitutively overexpress the L-selectin gene that can be transactivated by proteinHTLV-1 Tax .
These results indicated that ATL cells constitutively overexpress the L-selectin gene that can be transactivated by HTLV-1 proteinTax .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4188 20.2102 1.0000 The overexpression of L-selectin , as well as of inflammatory cytokines , by ATL cells may provide a basis for cell_lineATL cells to attach the vascular endothelium , leading to transmigration and organ infitration .
2.3677 20.6628 1.0000 The overexpression of L-selectin , as well as of proteininflammatory cytokines , by ATL cells may provide a basis for ATL cells to attach the vascular endothelium , leading to transmigration and organ infitration .
1.7573 10.2698 1.0000 The overexpression of proteinL-selectin , as well as of inflammatory cytokines , by ATL cells may provide a basis for ATL cells to attach the vascular endothelium , leading to transmigration and organ infitration .
1.6210 10.7793 1.0000 The overexpression of L-selectin , as well as of inflammatory cytokines , by cell_lineATL cells may provide a basis for ATL cells to attach the vascular endothelium , leading to transmigration and organ infitration .
0.6780 1.0000 1.0000 The overexpression of L-selectin , as well as of inflammatory proteincytokines , by ATL cells may provide a basis for ATL cells to attach the vascular endothelium , leading to transmigration and organ infitration .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0645 20.7991 10.1435 Human herpesvirus 6 variant A , but not variant B , infects EBV -positive B lymphoid cells , activating the DNAlatent EBV genome through a BZLF-1 -dependent mechanism .
0.8854 1.0000 1.0000 Human herpesvirus 6 variant A , but not variant B , infects EBV -positive B lymphoid cells , activating the latent EBV genome through a proteinBZLF-1 -dependent mechanism .
5.7125 30.0709 10.7223 Human herpesvirus 6 variant A , but not variant B , infects cell_typeEBV -positive B lymphoid cells , activating the latent EBV genome through a BZLF-1 -dependent mechanism .
Human herpesvirus 6 variant A , but not variant B , infects cell_lineEBV -positive B lymphoid cells , activating the latent EBV genome through a BZLF-1 -dependent mechanism .
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.1494 20.8285 20.3751 Human herpesvirus 6 , a predominantly T lymphotropic virus , has been recently shown to infect some cell_lineEBV -positive B cell lines , and to induce in them the activation of the EBV lytic cycle .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9662 20.6674 10.6223 Here we have confirmed and extended such observations, showing that (1) this phenomenon is restricted to the variant A of HHV-6 : in fact two isolates belonging to the HHV-6 variant B ( BA92 and Z29 ) were neither able to infect any cell_lineB cell line , independently of the EBV status , nor to induce the EBV genome expression .
2.9328 20.7245 10.4403 Here we have confirmed and extended such observations, showing that (1) this phenomenon is restricted to the variant A of HHV-6 : in fact two isolates belonging to the cell_lineHHV-6 variant B ( BA92 and Z29 ) were neither able to infect any B cell line , independently of the EBV status , nor to induce the EBV genome expression .
2.3028 20.9205 1.0000 Here we have confirmed and extended such observations, showing that (1) this phenomenon is restricted to the variant A of HHV-6 : in fact two isolates belonging to the HHV-6 variant B ( BA92 and Z29 ) were neither able to infect any B cell line , independently of the EBV status , nor to induce the DNAEBV genome expression .
0.9595 1.0000 1.0000 Here we have confirmed and extended such observations, showing that (1) this phenomenon is restricted to the variant A of HHV-6 : in fact two isolates belonging to the HHV-6 variant B ( BA92 and cell_lineZ29 ) were neither able to infect any B cell line , independently of the EBV status , nor to induce the EBV genome expression .
0.9544 1.0000 1.0000 Here we have confirmed and extended such observations, showing that (1) this phenomenon is restricted to the variant A of HHV-6 : in fact two isolates belonging to the HHV-6 variant B ( cell_lineBA92 and Z29 ) were neither able to infect any B cell line , independently of the EBV status , nor to induce the EBV genome expression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5003 20.2823 1.0000 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these DNApromoters .
2.3688 30.1687 1.0000 The only exception is represented by the cell_lineP3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
2.3097 20.6567 0.9999 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of cell_typeinfectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
2.2745 30.9205 0.9998 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the cell_lineB cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
2.2343 20.4695 1.0000 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of proteinEBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
2.1490 20.3573 1.0000 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the DNAEBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
1.4524 20.4528 0.9999 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the DNApromoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
0.9700 1.0000 1.0000 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and DNABMRF1 , show a strong transactivation of these promoters .
0.9547 0.9999 0.9998 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes DNABZLF1 and BMRF1 , show a strong transactivation of these promoters .
0.7765 1.0000 1.0000 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with DNAplasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
4.1746 30.8632 10.2002 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) cell_typeHHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
1.4773 0.9999 10.0617 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected cell_typeT cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
1.4164 10.9827 1.0000 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the DNAbinding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
0.7218 0.9977 0.9820 The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) HHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the DNAEBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
The only exception is represented by the P3HR1 cells , in which, however, the infection by the variant B does not determine induction of EBV antigens ; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection , increasing the binding sites and the percentage of infectable cells , as detected by immunoelectron microscopy ; and (3) cell_lineHHV-6 infected T cells , transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1 , show a strong transactivation of these promoters .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2534 20.7181 10.8398 Evidence for normal RNAvitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria .
3.0763 20.9367 10.5744 Evidence for normal proteinvitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.9832 30.9958 20.6431 Inasmuch as these features implicate enhanced calcitriol action in gut and bone , we analyzed the DNAvitamin D receptor ( VDR ) gene to ascertain whether an abnormality of this gene marks patients with intestinal hyperabsorption of calcium .
4.1264 30.9922 10.9751 Inasmuch as these features implicate enhanced calcitriol action in gut and bone , we analyzed the proteinvitamin D receptor ( VDR ) gene to ascertain whether an abnormality of this gene marks patients with intestinal hyperabsorption of calcium .
0.9375 1.0000 0.9891 Inasmuch as these features implicate enhanced calcitriol action in gut and bone , we analyzed the vitamin D receptor ( proteinVDR ) gene to ascertain whether an abnormality of this gene marks patients with intestinal hyperabsorption of calcium .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8317 30.1798 10.7238 We have compared the frequency of a DNArestriction fragment length polymorphism ( Bsm I ) associated with different alleles of the VDR gene in a group of 33 well characterized absorptive hypercalciuric patients and a group of 36 normal race- and age-matched control subjects .
1.5929 10.5890 1.0000 We have compared the frequency of a restriction fragment length polymorphism ( Bsm I ) associated with different alleles of the DNAVDR gene in a group of 33 well characterized absorptive hypercalciuric patients and a group of 36 normal race- and age-matched control subjects .
0.8491 0.9993 1.0000 We have compared the frequency of a restriction fragment length polymorphism ( DNABsm I ) associated with different alleles of the VDR gene in a group of 33 well characterized absorptive hypercalciuric patients and a group of 36 normal race- and age-matched control subjects .
0.6386 0.9999 1.0000 We have compared the frequency of a restriction fragment length polymorphism ( Bsm I ) associated with different DNAalleles of the VDR gene in a group of 33 well characterized absorptive hypercalciuric patients and a group of 36 normal race- and age-matched control subjects .
We have compared the frequency of a restriction fragment length polymorphism ( Bsm I ) associated with different alleles of the proteinVDR gene in a group of 33 well characterized absorptive hypercalciuric patients and a group of 36 normal race- and age-matched control subjects .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0649 20.2425 0.9890 There was no difference between the distribution of the proteinVDR alleles in the patient population when compared with the normal population .
2.3929 20.1938 1.0000 There was no difference between the distribution of the DNAVDR alleles in the patient population when compared with the normal population .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6893 10.5302 10.3432 The coding region of RNAVDR messenger RNA was also normal, as determined by both DNA sequence analysis and chemical mismatch cleavage analysis of copy DNA from 11 index absorptive hypercalciuric patients .
1.4116 10.7424 0.9960 The coding region of proteinVDR messenger RNA was also normal, as determined by both DNA sequence analysis and chemical mismatch cleavage analysis of copy DNA from 11 index absorptive hypercalciuric patients .
1.4099 10.2671 1.0000 The coding region of VDR messenger RNA was also normal, as determined by both DNADNA sequence analysis and chemical mismatch cleavage analysis of copy DNA from 11 index absorptive hypercalciuric patients .
2.2789 20.0983 1.0000 The coding region of VDR messenger RNA was also normal, as determined by both DNA sequence analysis and chemical mismatch cleavage analysis of DNAcopy DNA from 11 index absorptive hypercalciuric patients .
1.5458 10.5113 0.9999 The DNAcoding region of VDR messenger RNA was also normal, as determined by both DNA sequence analysis and chemical mismatch cleavage analysis of copy DNA from 11 index absorptive hypercalciuric patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9358 1.0000 1.0000 On the basis of these results, we propose that the enhanced intestinal calcium absorption invariably seen in absorptive hypercalciuria and attendant symptoms of this disorder are not attributable to mutations of the proteinVDR and are not linked to a common VDR genotype .
0.9059 1.0000 1.0000 On the basis of these results, we propose that the enhanced intestinal calcium absorption invariably seen in absorptive hypercalciuria and attendant symptoms of this disorder are not attributable to mutations of the VDR and are not linked to a common proteinVDR genotype .
On the basis of these results, we propose that the enhanced intestinal calcium absorption invariably seen in absorptive hypercalciuria and attendant symptoms of this disorder are not attributable to mutations of the VDR and are not linked to a common DNAVDR genotype .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1590 30.9401 10.5130 Transcriptional regulation of the gene encoding the proteinhuman C-type lectin leukocyte receptor AIM/CD69 and functional characterization of its tumor necrosis factor-alpha -responsive elements .
4.4261 30.5556 10.8921 Transcriptional regulation of the gene encoding the human C-type lectin leukocyte receptor AIM/CD69 and functional characterization of its DNAtumor necrosis factor-alpha -responsive elements .
2.5211 30.6375 10.8609 Transcriptional regulation of the gene encoding the human C-type lectin leukocyte receptor AIM/CD69 and functional characterization of its proteintumor necrosis factor-alpha -responsive elements .
0.9598 0.9999 1.0000 Transcriptional regulation of the gene encoding the human C-type lectin leukocyte receptor proteinAIM/CD69 and functional characterization of its tumor necrosis factor-alpha -responsive elements .
Transcriptional regulation of the gene encoding the human C-type lectin leukocyte receptor AIM/CD69 and functional characterization of its tumor necrosis factor-alpha -responsive DNAelements .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3232 20.9237 10.8769 The human activation antigen CD69 is a member of the proteinC-type animal lectin superfamily that functions as a signal-transmitting receptor .
1.8710 20.6477 0.9997 The human activation antigen CD69 is a member of the C-type animal lectin superfamily that functions as a proteinsignal-transmitting receptor .
0.8635 0.9997 1.0000 The human activation antigen proteinCD69 is a member of the C-type animal lectin superfamily that functions as a signal-transmitting receptor .
3.7879 10.9145 20.5229 The proteinhuman activation antigen CD69 is a member of the C-type animal lectin superfamily that functions as a signal-transmitting receptor .
The proteinhuman activation antigen CD69 is a member of the C-type animal lectin superfamily that functions as a signal-transmitting receptor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4923 20.8110 1.0000 Although the expression of CD69 can be induced in vitro on cells of most hematopoietic lineages with a wide variety of stimuli, in vivo it is mainly expressed by cell_typeT- lymphocytes located in the inflammatory infiltrates of several human diseases .
2.4827 20.2957 1.0000 Although the expression of proteinCD69 can be induced in vitro on cells of most hematopoietic lineages with a wide variety of stimuli, in vivo it is mainly expressed by T- lymphocytes located in the inflammatory infiltrates of several human diseases .
2.3471 20.4548 0.9999 Although the expression of CD69 can be induced in vitro on cells of most cell_typehematopoietic lineages with a wide variety of stimuli, in vivo it is mainly expressed by T- lymphocytes located in the inflammatory infiltrates of several human diseases .
2.2042 20.8112 0.9588 Although the expression of CD69 can be induced in vitro on cells of most hematopoietic lineages with a wide variety of stimuli, in vivo it is mainly expressed by cell_typeT- lymphocytes located in the inflammatory infiltrates of several human diseases .
Although the expression of CD69 can be induced in vitro on cells of most hematopoietic lineages with a wide variety of stimuli, in vivo it is mainly expressed by T- cell_typelymphocytes located in the inflammatory infiltrates of several human diseases .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3562 20.4586 0.9999 To elucidate the mechanisms that regulate the constitutive and inducible expression of CD69 by leukocytes , we isolated the DNApromoter region of the CD69 gene and carried out its functional characterization .
2.2185 20.4949 0.9944 To elucidate the mechanisms that regulate the constitutive and inducible expression of CD69 by leukocytes , we isolated the promoter region of the proteinCD69 gene and carried out its functional characterization .
1.6455 10.6893 1.0000 To elucidate the mechanisms that regulate the constitutive and inducible expression of proteinCD69 by leukocytes , we isolated the promoter region of the CD69 gene and carried out its functional characterization .
0.9027 1.0000 1.0000 To elucidate the mechanisms that regulate the constitutive and inducible expression of CD69 by cell_typeleukocytes , we isolated the promoter region of the CD69 gene and carried out its functional characterization .
2.3379 20.1921 1.0000 To elucidate the mechanisms that regulate the constitutive and inducible expression of CD69 by leukocytes , we isolated the promoter region of the DNACD69 gene and carried out its functional characterization .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1131 20.3698 1.0000 Sequence analysis of the 5'-flanking region of the DNACD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
2.0551 20.8674 0.9999 Sequence analysis of the DNA5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
2.0166 20.7401 0.9922 Sequence analysis of the 5'-flanking region of the proteinCD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
1.9781 20.7597 0.9972 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential DNATATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
1.6802 10.1245 1.0000 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( proteinNF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
1.4557 20.2051 10.5954 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible proteintranscription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
0.9770 1.0000 1.0000 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , proteinAP-1 ), which might mediate the inducible expression of this gene.
0.9758 1.0000 1.0000 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , proteinEgr-1 , AP-1 ), which might mediate the inducible expression of this gene.
0.6883 0.8680 0.9929 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element DNA30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
4.3470 20.9760 10.6215 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the DNAmajor transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
2.1118 10.3683 10.9534 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for proteininducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
2.0706 30.0866 10.7146 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential DNATATA element 30 base pairs upstream of the major transcription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
2.0420 20.4243 0.9998 Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major transcription initiation site and several putative DNAbinding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
Sequence analysis of the 5'-flanking region of the CD69 gene revealed the presence of a potential TATA element 30 base pairs upstream of the major DNAtranscription initiation site and several putative binding sequences for inducible transcription factors ( NF-kappa B , Egr-1 , AP-1 ), which might mediate the inducible expression of this gene.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9759 20.6856 10.7932 Transient expression of CD69 promoter-based reporter gene constructs in K562 cells indicated that the DNAproximal promoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
3.1185 30.3252 10.6817 Transient expression of DNACD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal promoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
2.1074 20.5600 0.9999 Transient expression of CD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal promoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the DNACD69 gene .
2.0137 20.9798 0.9974 Transient expression of proteinCD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal promoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
2.0107 20.2293 0.9999 Transient expression of CD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal promoter region spanning positions -78 to +16 contained the DNAcis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
1.5749 20.7317 0.9780 Transient expression of CD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal promoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the proteinCD69 gene .
1.4833 10.3116 0.9997 Transient expression of CD69 promoter-based reporter gene constructs in cell_lineK562 cells indicated that the proximal promoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
3.6776 20.4244 10.9868 Transient expression of CD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal promoter region spanning positions DNA-78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
Transient expression of CD69 promoter-based reporter gene constructs in K562 cells indicated that the proximal DNApromoter region spanning positions -78 to +16 contained the cis-acting sequences necessary for basal and phorbol 12-myristate 13-acetate -inducible transcription of the CD69 gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9851 10.9583 10.6296 Removal of the upstream sequences located between positions DNA-78 and -38 resulted in decreased promoter strength and abolished the response to phorbol 12-myristate 13-acetate.
2.2695 20.1204 1.0000 Removal of the DNAupstream sequences located between positions -78 and -38 resulted in decreased promoter strength and abolished the response to phorbol 12-myristate 13-acetate.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7215 20.6040 10.8992 We also found that proteintumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
2.0575 20.6608 0.9902 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the proteinCD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
1.5230 10.5987 1.0000 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of proteinCD69 .
1.5103 10.6449 1.0000 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the proteinCD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
0.9742 1.0000 1.0000 We also found that tumor necrosis factor-alpha ( proteinTNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
2.1760 20.0188 0.9999 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of DNAfusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
2.1754 20.0696 0.9999 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of fusion plasmids that contain DNA5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
2.1422 20.1684 1.0000 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the proteinCD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this cytokine may regulate in vivo the expression of CD69 .
0.8863 1.0000 1.0000 We also found that tumor necrosis factor-alpha ( TNF-alpha ) is capable of inducing the surface expression of the CD69 molecule as well as the promoter activity of fusion plasmids that contain 5'-flanking sequences of the CD69 gene, suggesting that this proteincytokine may regulate in vivo the expression of CD69 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3152 10.9733 10.3065 Characterization of 5' end of DNAhuman thromboxane receptor gene .
1.5602 10.9398 10.7542 Characterization of 5' end of proteinhuman thromboxane receptor gene .
1.1995 10.8267 0.9993 Characterization of DNA5' end of human thromboxane receptor gene .
Characterization of DNA5' end of human thromboxane receptor gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5378 20.1055 0.9999 Organizational analysis and mapping of DNAprotein kinase C--responsive elements regulating expression in platelets .
1.4394 10.3254 0.9999 Organizational analysis and mapping of protein kinase C--responsive elements regulating expression in cell_typeplatelets .
Organizational analysis and mapping of protein kinase C--responsive DNAelements regulating expression in platelets .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7754 0.9988 10.4490 proteinPlatelet thromboxane receptors are acutely and reversibly upregulated after acute myocardial infarction .
0.9876 0.9999 10.2241 Platelet proteinthromboxane receptors are acutely and reversibly upregulated after acute myocardial infarction .
cell_typePlatelet thromboxane receptors are acutely and reversibly upregulated after acute myocardial infarction .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3662 20.9601 10.6238 To determine if platelet thromboxane receptors are under transcriptional control , we isolated and characterized DNAhuman genomic DNA clones containing the 5' flanking region of the thromboxane receptor gene .
4.0992 30.9031 10.5507 To determine if platelet thromboxane receptors are under transcriptional control , we isolated and characterized human genomic DNA clones containing the DNA5' flanking region of the thromboxane receptor gene .
1.4397 20.5348 0.9993 To determine if platelet thromboxane receptors are under transcriptional control , we isolated and characterized human genomic DNA clones containing the 5' flanking region of the DNAthromboxane receptor gene .
0.6028 0.9999 0.9999 To determine if platelet proteinthromboxane receptors are under transcriptional control , we isolated and characterized human genomic DNA clones containing the 5' flanking region of the thromboxane receptor gene .
3.6326 20.6698 10.7402 To determine if proteinplatelet thromboxane receptors are under transcriptional control , we isolated and characterized human genomic DNA clones containing the 5' flanking region of the thromboxane receptor gene .
0.9832 20.4412 0.6103 To determine if platelet thromboxane receptors are under transcriptional control , we isolated and characterized human genomic DNA clones containing the 5' flanking region of the proteinthromboxane receptor gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.8706 30.2481 10.4164 The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the DNA5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
2.1175 20.8154 0.9998 The exon-intron structure of the 5' portion of the DNAthromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
1.8906 20.7225 0.9999 The exon-intron structure of the DNA5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
1.8372 10.9121 10.1730 The DNAexon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
0.8165 1.0000 0.9156 The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine proteinthromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
5.0753 30.1318 10.6460 The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel DNAhuman uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
3.9972 30.2293 10.9400 The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified DNAhuman placental cDNA .
2.0588 20.6851 10.7753 The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the DNAmRNA 141 bp further upstream than the previously identified human placental cDNA .
The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a DNAnovel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
The exon-intron structure of the 5' portion of the proteinthromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the DNAnucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the previously identified human placental cDNA .
The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA 141 bp further upstream than the DNApreviously identified human placental cDNA .
The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the RNAmRNA 141 bp further upstream than the previously identified human placental cDNA .
The exon-intron structure of the 5' portion of the thromboxane receptor gene was determined initially by comparing the nucleotide sequence of the 5' flanking genomic clone with that of a novel human uterine thromboxane receptor cDNA that extended the mRNA DNA141 bp further upstream than the previously identified human placental cDNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1008 20.8402 10.6367 A major transcription initiation site was located in three human tissues approximately 560 bp upstream from the translation initiation codon and 380 bp upstream from any previously identified DNAtranscription initiation site .
4.0924 20.9483 10.6414 A major transcription initiation site was located in three human tissues approximately DNA560 bp upstream from the translation initiation codon and 380 bp upstream from any previously identified transcription initiation site .
3.3397 20.2644 10.8963 A major transcription initiation site was located in three human tissues approximately 560 bp upstream from the DNAtranslation initiation codon and 380 bp upstream from any previously identified transcription initiation site .
2.8957 10.5802 10.5550 A major transcription initiation site was located in three human tissues approximately 560 bp upstream from the translation initiation codon and DNA380 bp upstream from any previously identified transcription initiation site .
2.6419 20.9799 10.7751 A major DNAtranscription initiation site was located in three human tissues approximately 560 bp upstream from the translation initiation codon and 380 bp upstream from any previously identified transcription initiation site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1456 20.4246 10.5149 The thromboxane receptor gene has neither a TATA nor a DNACAAT consensus site .
2.3062 10.8334 10.1722 The DNAthromboxane receptor gene has neither a TATA nor a CAAT consensus site .
0.5637 0.9835 0.3199 The proteinthromboxane receptor gene has neither a TATA nor a CAAT consensus site .
The thromboxane receptor gene has neither a DNATATA nor a CAAT consensus site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1000 30.2475 10.8183 Promoter function of the DNA5' flanking region of the thromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
2.9288 30.7589 10.3037 Promoter function of the 5' flanking region of the DNAthromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
0.9352 1.0000 0.9887 Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( proteinCAT ) chimera plasmids into platelet-like K562 cells .
0.9002 1.0000 0.9943 Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ proteinchloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
0.7834 0.7837 0.8292 Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of DNAthromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
2.6648 20.1245 10.2591 Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into cell_lineplatelet-like K562 cells .
Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of DNAthromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
Promoter function of the 5' flanking region of the proteinthromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of proteinthromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like K562 cells .
Promoter function of the 5' flanking region of the thromboxane receptor gene was evaluated by transfection of thromboxane receptor gene promoter/ chloramphenicol acetyltransferase ( CAT ) chimera plasmids into platelet-like cell_lineK562 cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7464 10.6142 1.0000 Thromboxane receptor promoter activity , as assessed by proteinCAT expression , was relatively weak but was significantly enhanced by phorbol ester treatment .
0.8974 0.9995 0.9997 proteinThromboxane receptor promoter activity , as assessed by CAT expression , was relatively weak but was significantly enhanced by phorbol ester treatment .
Thromboxane DNAreceptor promoter activity , as assessed by CAT expression , was relatively weak but was significantly enhanced by phorbol ester treatment .
Cls_Score Left_Reg_Score Right_Reg_Score Text
7.1138 30.6003 20.5690 Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of DNAactivator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
3.6434 20.6878 10.9715 Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the DNAtranscription initiation site .
2.5107 30.4161 10.3006 Functional analysis of DNA5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
1.6739 20.0291 0.8706 Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the proteinthromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
0.9666 1.0000 0.9980 Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of activator protein-2 ( proteinAP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
5.0725 30.0898 10.9133 Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the DNAthromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
2.6941 20.0297 10.6124 Functional analysis of 5' deletion constructs in cell_linetransfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
2.5665 30.0070 10.8440 Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major DNAphorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
Functional analysis of 5' deletion constructs in transfected cell_lineK562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the thromboxane receptor gene promoter to a cluster of proteinactivator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
Functional analysis of 5' deletion constructs in transfected K562 cells and gel mobility shift localized the major phorbol ester -responsive motifs in the DNAthromboxane receptor gene promoter to a cluster of activator protein-2 ( AP-2 ) binding consensus sites located approximately 1.8 kb 5' from the transcription initiation site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6944 20.8287 10.9485 These studies are the first to determine the structure and organization of the 5' end of the thromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an proteinAP-2 -like nuclear factor binding to upstream promoter elements .
4.1891 30.8986 10.8051 These studies are the first to determine the structure and organization of the 5' end of the thromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an AP-2 -like nuclear factor binding to DNAupstream promoter elements .
3.5422 20.5917 10.7822 These studies are the first to determine the structure and organization of the 5' end of the thromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of proteinprotein kinase C via induction of an AP-2 -like nuclear factor binding to upstream promoter elements .
2.2897 20.8102 0.9998 These studies are the first to determine the structure and organization of the 5' end of the DNAthromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an AP-2 -like nuclear factor binding to upstream promoter elements .
2.0842 20.2274 0.9999 These studies are the first to determine the structure and organization of the 5' end of the thromboxane receptor gene and demonstrate that proteinthromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an AP-2 -like nuclear factor binding to upstream promoter elements .
1.5501 20.7642 0.6077 These studies are the first to determine the structure and organization of the 5' end of the proteinthromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an AP-2 -like nuclear factor binding to upstream promoter elements .
0.7793 1.0000 0.9990 These studies are the first to determine the structure and organization of the 5' end of the thromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an proteinAP-2 -like nuclear factor binding to upstream promoter elements .
2.0836 20.5095 0.9999 These studies are the first to determine the structure and organization of the DNA5' end of the thromboxane receptor gene and demonstrate that thromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an AP-2 -like nuclear factor binding to upstream promoter elements .
These studies are the first to determine the structure and organization of the 5' end of the thromboxane receptor gene and demonstrate that DNAthromboxane receptor gene expression can be regulated by activation of protein kinase C via induction of an AP-2 -like nuclear factor binding to upstream promoter elements .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3994 20.3164 0.9998 These findings strongly suggest that the mechanism for previously described upregulation of platelet thromboxane receptors after acute myocardial infarction is increased thromboxane receptor gene transcription in cell_typeplatelet-progenitor cells .
2.2278 20.5867 0.9999 These findings strongly suggest that the mechanism for previously described upregulation of platelet thromboxane receptors after acute myocardial infarction is increased proteinthromboxane receptor gene transcription in platelet-progenitor cells .
2.1274 20.9820 0.9999 These findings strongly suggest that the mechanism for previously described upregulation of proteinplatelet thromboxane receptors after acute myocardial infarction is increased thromboxane receptor gene transcription in platelet-progenitor cells .
1.5726 20.6268 0.9960 These findings strongly suggest that the mechanism for previously described upregulation of cell_typeplatelet thromboxane receptors after acute myocardial infarction is increased thromboxane receptor gene transcription in platelet-progenitor cells .
0.7601 0.9996 0.9999 These findings strongly suggest that the mechanism for previously described upregulation of platelet proteinthromboxane receptors after acute myocardial infarction is increased thromboxane receptor gene transcription in platelet-progenitor cells .
These findings strongly suggest that the mechanism for previously described upregulation of platelet thromboxane receptors after acute myocardial infarction is increased DNAthromboxane receptor gene transcription in platelet-progenitor cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9168 0.9996 1.0000 proteinEstrogen receptor concentration and social factors as predictors of natural killer cell activity in early-stage breast cancer patients .
3.6873 20.7632 10.6405 Estrogen receptor concentration and social factors as predictors of cell_typenatural killer cell activity in early-stage breast cancer patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6880 20.2111 1.0000 Previous work of ours has demonstrated that a significant amount of natural killer (NK) activity variance after surgery in stage I and II breast cancer patients could be accounted for by both the proteinestrogen receptor ( ER ) status of the tumor and by social factors , namely, perceived social support and seeking social support as a general coping strategy .
0.9886 1.0000 1.0000 Previous work of ours has demonstrated that a significant amount of natural killer (NK) activity variance after surgery in stage I and II breast cancer patients could be accounted for by both the estrogen receptor ( proteinER ) status of the tumor and by social factors , namely, perceived social support and seeking social support as a general coping strategy .
1.5245 20.5689 0.9988 Previous work of ours has demonstrated that a significant amount of cell_typenatural killer (NK) activity variance after surgery in stage I and II breast cancer patients could be accounted for by both the estrogen receptor ( ER ) status of the tumor and by social factors , namely, perceived social support and seeking social support as a general coping strategy .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9614 1.0000 1.0000 It was found that the most significant variable predicting NK activity at follow-up was tumor proteinER concentration , with higher NK activity associated with ER -status .
0.9284 1.0000 1.0000 It was found that the most significant variable predicting NK activity at follow-up was tumor ER concentration , with higher NK activity associated with proteinER -status .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6149 20.7858 1.0000 If, as the literature suggests, NK activity is relevant to breast cancer control , and since ER -tumors have a worse prognosis, we suggest here that perhaps such tumors are resistant to control by NK cells because they lack the ability to attract an accumulation of cell_typeeffector cells to the tumor site , or because blocking factors at the site of the tumor prevent local tumor control at the site of action.
2.6038 20.7511 1.0000 If, as the literature suggests, NK activity is relevant to breast cancer control , and since ER -tumors have a worse prognosis, we suggest here that perhaps such tumors are resistant to control by cell_typeNK cells because they lack the ability to attract an accumulation of effector cells to the tumor site , or because blocking factors at the site of the tumor prevent local tumor control at the site of action.
0.6636 1.0000 1.0000 If, as the literature suggests, NK activity is relevant to breast cancer control , and since ER -tumors have a worse prognosis, we suggest here that perhaps such tumors are resistant to control by NK cells because they lack the ability to attract an accumulation of effector cells to the tumor site , or because blocking proteinfactors at the site of the tumor prevent local tumor control at the site of action.
If, as the literature suggests, NK activity is relevant to breast cancer control , and since proteinER -tumors have a worse prognosis, we suggest here that perhaps such tumors are resistant to control by NK cells because they lack the ability to attract an accumulation of effector cells to the tumor site , or because blocking factors at the site of the tumor prevent local tumor control at the site of action.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1561 20.3135 10.7457 Solution structure of the sequence-specific HMG box of the proteinlymphocyte transcriptional activator Sox-4 .
0.9673 1.0000 0.9999 Solution structure of the sequence-specific HMG box of the lymphocyte transcriptional activator proteinSox-4 .
3.2227 20.3067 10.7378 Solution structure of the proteinsequence-specific HMG box of the lymphocyte transcriptional activator Sox-4 .
Solution structure of the DNAsequence-specific HMG box of the lymphocyte transcriptional activator Sox-4 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.7224 10.7033 10.9160 Two groups of proteinHMG box proteins are distinguished.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2138 20.3890 1.0000 Proteins in the first group contain multiple HMG boxes , are non-sequence-specific , and recognize structural features as found in DNAcruciform DNA and cross-over DNA .
1.0691 10.6448 0.9997 Proteins in the first group contain multiple HMG boxes , are non-sequence-specific , and recognize structural features as found in cruciform DNA and DNAcross-over DNA .
0.6181 0.9999 0.9999 Proteins in the first group contain multiple proteinHMG boxes , are non-sequence-specific , and recognize structural features as found in cruciform DNA and cross-over DNA .
3.3565 20.8573 10.3580 Proteins in the first group contain proteinmultiple HMG boxes , are non-sequence-specific , and recognize structural features as found in cruciform DNA and cross-over DNA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8101 10.9120 10.7363 The abundant proteinchromosomal protein HMG-1 belongs to this subgroup.
The abundant chromosomal protein proteinHMG-1 belongs to this subgroup.
The abundant proteinchromosomal protein HMG-1 belongs to this subgroup.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8672 20.1775 1.0000 Proteins in the second group carry a single HMG box with affinity for the DNAminor groove of the heptamer motif AACAAAG or variations thereof.
1.6861 20.0583 1.0000 Proteins in the second group carry a single HMG box with affinity for the minor groove of the DNAheptamer motif AACAAAG or variations thereof.
1.5680 10.8600 1.0000 Proteins in the second group carry a single proteinHMG box with affinity for the minor groove of the heptamer motif AACAAAG or variations thereof.
Proteins in the second group carry a proteinsingle HMG box with affinity for the minor groove of the heptamer motif AACAAAG or variations thereof.
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9086 1.0000 1.0000 A solution structure for the non-sequence-specific C-terminal HMG box of proteinHMG-1 has recently been proposed.
3.7253 20.7450 10.9377 A solution structure for the proteinnon-sequence-specific C-terminal HMG box of HMG-1 has recently been proposed.
A solution structure for the non-sequence-specific proteinC-terminal HMG box of HMG-1 has recently been proposed.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.3794 10.7994 0.9991 Now, we report the solution structure of the sequence-specific HMG-box of the proteinSRY-related protein Sox-4 .
1.3689 10.9738 0.9999 Now, we report the solution structure of the proteinsequence-specific HMG-box of the SRY-related protein Sox-4 .
0.9615 1.0000 1.0000 Now, we report the solution structure of the sequence-specific HMG-box of the SRY-related protein proteinSox-4 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6449 10.8286 1.0000 NMR analysis demonstrated the presence of three proteinalpha-helices ( Val10-Gln22 , Glu30-Leu41 and Phe50-Tyr65 ) connected by loop regions ( Ser23-Ala49 and Leu42-Pro49 ).
1.5358 10.9710 1.0000 NMR analysis demonstrated the presence of three alpha-helices ( Val10-Gln22 , Glu30-Leu41 and Phe50-Tyr65 ) connected by proteinloop regions ( Ser23-Ala49 and Leu42-Pro49 ).
0.7587 1.0000 1.0000 NMR analysis demonstrated the presence of three alpha-helices ( Val10-Gln22 , Glu30-Leu41 and proteinPhe50-Tyr65 ) connected by loop regions ( Ser23-Ala49 and Leu42-Pro49 ).
0.5840 1.0000 1.0000 NMR analysis demonstrated the presence of three alpha-helices ( Val10-Gln22 , Glu30-Leu41 and Phe50-Tyr65 ) connected by loop regions ( proteinSer23-Ala49 and Leu42-Pro49 ).
0.5423 0.9999 1.0000 NMR analysis demonstrated the presence of three alpha-helices ( Val10-Gln22 , proteinGlu30-Leu41 and Phe50-Tyr65 ) connected by loop regions ( Ser23-Ala49 and Leu42-Pro49 ).
NMR analysis demonstrated the presence of three alpha-helices ( Val10-Gln22 , Glu30-Leu41 and Phe50-Tyr65 ) connected by loop regions ( Ser23-Ala49 and proteinLeu42-Pro49 ).
NMR analysis demonstrated the presence of three alpha-helices ( proteinVal10-Gln22 , Glu30-Leu41 and Phe50-Tyr65 ) connected by loop regions ( Ser23-Ala49 and Leu42-Pro49 ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3519 20.7014 0.9999 Helices I and II are positioned in an antiparallel mode and form one arm of the proteinHMG box .
Helices I and II are positioned in an proteinantiparallel mode and form one arm of the HMG box .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9364 1.0000 1.0000 proteinHelix III is less rigid, makes an average angle of about 90 degrees with helices I and II , and constitutes the other arm of the molecule.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4279 20.1162 1.0000 As in proteinHMG1B , the overall structure of the Sox-4 HMG box is L-shaped and is maintained by a cluster of conserved, mainly aromatic residues .
3.8496 20.8832 10.3333 As in HMG1B , the overall structure of the proteinSox-4 HMG box is L-shaped and is maintained by a cluster of conserved, mainly aromatic residues .
As in HMG1B , the overall structure of the Sox-4 proteinHMG box is L-shaped and is maintained by a cluster of conserved, mainly aromatic residues .
As in HMG1B , the overall structure of the proteinSox-4 HMG box is L-shaped and is maintained by a cluster of conserved, mainly aromatic residues .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2468 20.0634 10.6048 Nuclear factor-IL6 activates the DNAhuman IL-4 promoter in T cells .
1.3447 10.7435 0.9993 Nuclear factor-IL6 activates the human IL-4 promoter in cell_typeT cells .
0.8143 0.9980 0.9999 proteinNuclear factor-IL6 activates the human IL-4 promoter in T cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3816 30.1346 10.6003 Positive regulatory element I ( PRE-I ) is a strong enhancer element essential for expression of the DNAhuman IL-4 gene .
1.7103 20.9956 0.9999 Positive regulatory element I ( PRE-I ) is a strong DNAenhancer element essential for expression of the human IL-4 gene .
1.4327 0.9810 10.1628 DNAPositive regulatory element I ( PRE-I ) is a strong enhancer element essential for expression of the human IL-4 gene .
0.9482 1.0000 1.0000 Positive regulatory element I ( DNAPRE-I ) is a strong enhancer element essential for expression of the human IL-4 gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0930 20.3921 10.8569 To identify transcription factors binding to PRE-I , we screened a DNAcDNA expression library from Jurkat T cells and isolated a cDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
2.8848 10.8842 10.9802 To identify transcription factors binding to PRE-I , we screened a cDNA expression library from cell_lineJurkat T cells and isolated a cDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
1.5649 10.4846 1.0000 To identify transcription factors binding to DNAPRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a cDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
1.3395 10.7325 1.0000 To identify proteintranscription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a cDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
1.2559 10.8642 0.9999 To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a cDNA encoding nuclear factor (NF)-IL6 (also known as proteinC/EBP beta ).
4.5093 20.7126 10.8975 To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a proteincDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
1.2439 0.9998 10.0225 To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a cDNA encoding proteinnuclear factor (NF)-IL6 (also known as C/EBP beta ).
To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a cDNA encoding nuclear factor protein(NF)-IL6 (also known as C/EBP beta ).
To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a DNAcDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat T cells and isolated a cDNA encoding proteinnuclear factor (NF)-IL6 (also known as C/EBP beta ).
To identify transcription factors binding to PRE-I , we screened a cDNA expression library from Jurkat cell_typeT cells and isolated a cDNA encoding nuclear factor (NF)-IL6 (also known as C/EBP beta ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4180 20.8097 10.7198 NF-IL6 mRNA was found in human Jurkat T cells and in the mouse Th2 clone D10 , but not in cell_lineTh1 clone 29 .
0.8722 0.9953 1.0000 RNANF-IL6 mRNA was found in human Jurkat T cells and in the mouse Th2 clone D10 , but not in Th1 clone 29 .
4.4698 20.6832 10.8080 NF-IL6 mRNA was found in human Jurkat T cells and in the cell_linemouse Th2 clone D10 , but not in Th1 clone 29 .
3.4016 20.3300 10.8206 NF-IL6 mRNA was found in human cell_lineJurkat T cells and in the mouse Th2 clone D10 , but not in Th1 clone 29 .
0.8995 0.9999 0.9872 proteinNF-IL6 mRNA was found in human Jurkat T cells and in the mouse Th2 clone D10 , but not in Th1 clone 29 .
NF-IL6 mRNA was found in human Jurkat T cells and in the mouse Th2 clone cell_lineD10 , but not in Th1 clone 29 .
NF-IL6 mRNA was found in human Jurkat T cells and in the cell_linemouse Th2 clone D10 , but not in Th1 clone 29 .
NF-IL6 mRNA was found in human Jurkat cell_typeT cells and in the mouse Th2 clone D10 , but not in Th1 clone 29 .
NF-IL6 mRNA was found in cell_linehuman Jurkat T cells and in the mouse Th2 clone D10 , but not in Th1 clone 29 .
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1.5752 10.6608 1.0000 rNF-IL6 expressed in bacteria was shown to specifically bind to DNAPRE-I .
0.9801 1.0000 1.0000 proteinrNF-IL6 expressed in bacteria was shown to specifically bind to PRE-I .
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2.0887 20.0327 0.9997 PRE-I forms multiple DNA-protein complexes with nuclear extracts from cell_lineJurkat cells .
0.9308 0.9999 1.0000 DNAPRE-I forms multiple DNA-protein complexes with nuclear extracts from Jurkat cells .
2.6824 20.3012 10.0478 PRE-I forms multiple proteinDNA-protein complexes with nuclear extracts from Jurkat cells .
PRE-I forms proteinmultiple DNA-protein complexes with nuclear extracts from Jurkat cells .
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3.8425 20.1044 10.7776 Some of these complexes were demonstrated to contain NF-IL6 by using proteinanti- C/EBP beta Abs .
1.4020 10.8857 1.0000 Some of these complexes were demonstrated to contain proteinNF-IL6 by using anti- C/EBP beta Abs .
0.6815 1.0000 0.8547 Some of these complexes were demonstrated to contain NF-IL6 by using anti- proteinC/EBP beta Abs .
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4.6889 20.7842 10.9086 Overexpression of NF-IL6 enhanced expression of the DNAchloramphenicol acetyl transferase reporter gene linked to the PRE-I -thymidine kinase or the human IL-4 promoter more than 10-fold in Jurkat cells .
3.8709 40.3262 10.4592 Overexpression of NF-IL6 enhanced expression of the chloramphenicol acetyl transferase reporter gene linked to the proteinPRE-I -thymidine kinase or the human IL-4 promoter more than 10-fold in Jurkat cells .
3.4266 20.9725 10.7632 Overexpression of NF-IL6 enhanced expression of the chloramphenicol acetyl transferase reporter gene linked to the PRE-I -thymidine kinase or the DNAhuman IL-4 promoter more than 10-fold in Jurkat cells .
2.7116 30.8442 10.6369 Overexpression of NF-IL6 enhanced expression of the proteinchloramphenicol acetyl transferase reporter gene linked to the PRE-I -thymidine kinase or the human IL-4 promoter more than 10-fold in Jurkat cells .
2.0973 20.0565 1.0000 Overexpression of proteinNF-IL6 enhanced expression of the chloramphenicol acetyl transferase reporter gene linked to the PRE-I -thymidine kinase or the human IL-4 promoter more than 10-fold in Jurkat cells .
1.2891 10.4135 0.9991 Overexpression of NF-IL6 enhanced expression of the chloramphenicol acetyl transferase reporter gene linked to the PRE-I -thymidine kinase or the human IL-4 promoter more than 10-fold in cell_lineJurkat cells .
Overexpression of NF-IL6 enhanced expression of the chloramphenicol acetyl transferase reporter gene linked to the PRE-I -thymidine kinase or the proteinhuman IL-4 promoter more than 10-fold in Jurkat cells .
Overexpression of NF-IL6 enhanced expression of the chloramphenicol acetyl transferase reporter gene linked to the DNAPRE-I -thymidine kinase or the human IL-4 promoter more than 10-fold in Jurkat cells .
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3.5986 20.9490 10.8084 Promoter deletion studies revealed two additional DNANF-IL6 binding sites located at positions -44 to -36 ( C/EBP proximal ) and -87 to -79 ( C/EBP medial ), respectively.
2.0559 20.3084 0.9957 Promoter deletion studies revealed two additional proteinNF-IL6 binding sites located at positions -44 to -36 ( C/EBP proximal ) and -87 to -79 ( C/EBP medial ), respectively.
4.1098 20.1942 10.6972 Promoter deletion studies revealed two additional NF-IL6 binding sites located at positions DNA-44 to -36 ( C/EBP proximal ) and -87 to -79 ( C/EBP medial ), respectively.
3.4427 20.2255 10.7239 Promoter deletion studies revealed two additional NF-IL6 binding sites located at positions -44 to -36 ( C/EBP proximal ) and DNA-87 to -79 ( C/EBP medial ), respectively.
1.5285 10.1827 0.9999 Promoter deletion studies revealed two additional NF-IL6 binding sites located at positions -44 to -36 ( C/EBP proximal ) and -87 to -79 ( DNAC/EBP medial ), respectively.
1.5246 10.2299 0.9999 Promoter deletion studies revealed two additional NF-IL6 binding sites located at positions -44 to -36 ( DNAC/EBP proximal ) and -87 to -79 ( C/EBP medial ), respectively.
Promoter deletion studies revealed two additional NF-IL6 binding sites located at positions -44 to -36 ( proteinC/EBP proximal ) and -87 to -79 ( C/EBP medial ), respectively.
Promoter deletion studies revealed two additional NF-IL6 binding sites located at positions -44 to -36 ( C/EBP proximal ) and -87 to -79 ( proteinC/EBP medial ), respectively.
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2.4257 20.1996 0.9999 Our results demonstrate that NF-IL6 is involved in transcriptional activation of the DNAhuman IL-4 promoter in T cells .
1.5217 10.4199 0.9995 Our results demonstrate that NF-IL6 is involved in transcriptional activation of the human IL-4 promoter in cell_typeT cells .
1.5195 10.3223 1.0000 Our results demonstrate that proteinNF-IL6 is involved in transcriptional activation of the human IL-4 promoter in T cells .
0.8421 1.0000 0.9818 Our results demonstrate that NF-IL6 is involved in transcriptional activation of the human proteinIL-4 promoter in T cells .
Our results demonstrate that NF-IL6 is involved in transcriptional activation of the proteinhuman IL-4 promoter in T cells .
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5.3886 20.7123 20.1140 Identification of an proteinI kappa B alpha-associated protein kinase in a human monocytic cell line and determination of its phosphorylation sites on I kappa B alpha .
4.4077 30.4965 10.8411 Identification of an I kappa B alpha-associated protein kinase in a cell_linehuman monocytic cell line and determination of its phosphorylation sites on I kappa B alpha .
2.1700 20.6507 10.0789 Identification of an I kappa B alpha-associated protein kinase in a human monocytic cell line and determination of its phosphorylation sites on proteinI kappa B alpha .
1.8636 20.2324 0.9999 Identification of an I kappa B alpha-associated protein kinase in a human monocytic cell line and determination of its proteinphosphorylation sites on I kappa B alpha .
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3.4342 20.8772 10.9274 Nuclear factor kappa B ( NF-kappa B ) is stored in the cytoplasm as an inactive form through interaction with proteinI kappa B .
1.6679 10.5657 1.0000 Nuclear factor kappa B ( proteinNF-kappa B ) is stored in the cytoplasm as an inactive form through interaction with I kappa B .
1.6290 0.9967 10.3309 proteinNuclear factor kappa B ( NF-kappa B ) is stored in the cytoplasm as an inactive form through interaction with I kappa B .
2.1313 20.0266 1.0000 Nuclear factor kappa B ( NF-kappa B ) is stored in the cytoplasm as an proteininactive form through interaction with I kappa B .
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4.7478 20.3845 20.3963 Stimulation of cells leads to a rapid phosphorylation of proteinI kappa B alpha , which is presumed to be important for the subsequent degradation .
Stimulation of cells leads to a rapid phosphorylation of proteinI kappa B alpha , which is presumed to be important for the subsequent degradation .
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4.0130 20.7285 10.7072 We have recently reported the establishment of a lipopolysaccharide ( LPS )-dependent cell-free activation system of NF-kappa B in association with the induction of proteinI kappa B alpha phosphorylation .
1.5018 10.8983 1.0000 We have recently reported the establishment of a lipopolysaccharide ( LPS )-dependent cell-free activation system of proteinNF-kappa B in association with the induction of I kappa B alpha phosphorylation .
We have recently reported the establishment of a lipopolysaccharide ( LPS )-dependent cell-free activation system of NF-kappa B in association with the induction of proteinI kappa B alpha phosphorylation .
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8.1812 30.8593 20.5925 In this study, we have identified a kinase in cell extracts from the cell_lineLPS -stimulated human monocytic cell line , THP-1 , that specifically binds and phosphorylates I kappa B alpha .
3.7996 30.0775 10.1045 In this study, we have identified a kinase in cell extracts from the LPS -stimulated human monocytic cell line , THP-1 , that specifically binds and phosphorylates proteinI kappa B alpha .
0.9259 1.0000 1.0000 In this study, we have identified a kinase in cell extracts from the LPS -stimulated human monocytic cell line , cell_lineTHP-1 , that specifically binds and phosphorylates I kappa B alpha .
In this study, we have identified a proteinkinase in cell extracts from the LPS -stimulated human monocytic cell line , THP-1 , that specifically binds and phosphorylates I kappa B alpha .
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3.7178 20.8206 10.9166 LPS stimulation transiently enhanced the proteinI kappa B alpha -bound kinase activity in THP-1 cells .
2.0920 20.4326 0.9997 LPS stimulation transiently enhanced the I kappa B alpha -bound kinase activity in cell_lineTHP-1 cells .
LPS stimulation transiently enhanced the proteinI kappa B alpha -bound kinase activity in THP-1 cells .
LPS stimulation transiently enhanced the I kappa B alpha protein-bound kinase activity in THP-1 cells .
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4.0315 20.0676 10.6325 Mutational analyses of I kappa B alpha and competition experiments with the synthetic peptides identified major phosphorylation sites by the bound kinase as Ser and Thr residues in the C-terminal acidic domain of proteinI kappa B alpha .
2.7959 20.9992 10.9841 Mutational analyses of I kappa B alpha and competition experiments with the synthetic peptides identified major phosphorylation sites by the bound kinase as Ser and Thr residues in the proteinC-terminal acidic domain of I kappa B alpha .
0.8667 1.0000 1.0000 Mutational analyses of I kappa B alpha and competition experiments with the synthetic peptides identified major phosphorylation sites by the bound proteinkinase as Ser and Thr residues in the C-terminal acidic domain of I kappa B alpha .
5.3226 30.0301 10.6918 Mutational analyses of proteinI kappa B alpha and competition experiments with the synthetic peptides identified major phosphorylation sites by the bound kinase as Ser and Thr residues in the C-terminal acidic domain of I kappa B alpha .
3.1633 20.4873 10.8125 Mutational analyses of I kappa B alpha and competition experiments with the synthetic peptides identified proteinmajor phosphorylation sites by the bound kinase as Ser and Thr residues in the C-terminal acidic domain of I kappa B alpha .
Mutational analyses of I kappa B alpha and competition experiments with the synthetic peptides identified major proteinphosphorylation sites by the bound kinase as Ser and Thr residues in the C-terminal acidic domain of I kappa B alpha .
Mutational analyses of I kappa B alpha and competition experiments with the synthetic peptides identified major phosphorylation sites by the bound kinase as Ser and Thr residues in the C-terminal acidic domain of proteinI kappa B alpha .
Mutational analyses of proteinI kappa B alpha and competition experiments with the synthetic peptides identified major phosphorylation sites by the bound kinase as Ser and Thr residues in the C-terminal acidic domain of I kappa B alpha .
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4.7718 20.8882 10.6058 Moreover, we show that the peptide , corresponding to the C-terminal acidic domain of I kappa B alpha , blocked the LPS -induced NF-kappa B activation as well as inducible phosphorylation of endogenous proteinI kappa B alpha in a cell-free system using THP-1 cells .
4.2977 20.9968 10.6173 Moreover, we show that the peptide , corresponding to the proteinC-terminal acidic domain of I kappa B alpha , blocked the LPS -induced NF-kappa B activation as well as inducible phosphorylation of endogenous I kappa B alpha in a cell-free system using THP-1 cells .
3.3157 10.6721 10.6274 Moreover, we show that the peptide , corresponding to the C-terminal acidic domain of proteinI kappa B alpha , blocked the LPS -induced NF-kappa B activation as well as inducible phosphorylation of endogenous I kappa B alpha in a cell-free system using THP-1 cells .
2.1421 20.0532 0.9997 Moreover, we show that the peptide , corresponding to the C-terminal acidic domain of I kappa B alpha , blocked the LPS -induced NF-kappa B activation as well as inducible phosphorylation of endogenous I kappa B alpha in a cell-free system using cell_lineTHP-1 cells .
1.4985 10.7264 1.0000 Moreover, we show that the peptide , corresponding to the C-terminal acidic domain of I kappa B alpha , blocked the LPS -induced proteinNF-kappa B activation as well as inducible phosphorylation of endogenous I kappa B alpha in a cell-free system using THP-1 cells .
Moreover, we show that the peptide , corresponding to the C-terminal acidic domain of proteinI kappa B alpha , blocked the LPS -induced NF-kappa B activation as well as inducible phosphorylation of endogenous I kappa B alpha in a cell-free system using THP-1 cells .
Moreover, we show that the peptide , corresponding to the C-terminal acidic domain of I kappa B alpha , blocked the LPS -induced NF-kappa B activation as well as inducible phosphorylation of endogenous proteinI kappa B alpha in a cell-free system using THP-1 cells .
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4.0027 20.8759 10.9666 These results suggested that the bound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of proteinI kappa B alpha and subsequent dissociation of the NF-kappa B . I kappa B alpha complex .
3.3613 10.9550 10.4656 These results suggested that the bound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of I kappa B alpha and subsequent dissociation of the NF-kappa B . proteinI kappa B alpha complex .
2.1039 20.1247 0.9999 These results suggested that the bound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the proteinC-terminal region of I kappa B alpha and subsequent dissociation of the NF-kappa B . I kappa B alpha complex .
1.4306 10.0238 10.8705 These results suggested that the bound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of I kappa B alpha and subsequent dissociation of the NF-kappa B . proteinI kappa B alpha complex .
1.4102 10.4713 0.9996 These results suggested that the bound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of I kappa B alpha and subsequent dissociation of the proteinNF-kappa B . I kappa B alpha complex .
1.2100 10.0201 1.0000 These results suggested that the bound proteinkinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of I kappa B alpha and subsequent dissociation of the NF-kappa B . I kappa B alpha complex .
These results suggested that the proteinbound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of I kappa B alpha and subsequent dissociation of the NF-kappa B . I kappa B alpha complex .
These results suggested that the bound kinase is involved in the signaling pathway of LPS by inducing the phosphorylation of the C-terminal region of proteinI kappa B alpha and subsequent dissociation of the NF-kappa B . I kappa B alpha complex .
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3.6637 20.9546 10.4964 Bik , a novel death-inducing protein shares a distinct sequence motif with proteinBcl-2 family proteins and interacts with viral and cellular survival-promoting proteins .
2.0848 20.2401 0.9999 Bik , a novel proteindeath-inducing protein shares a distinct sequence motif with Bcl-2 family proteins and interacts with viral and cellular survival-promoting proteins .
0.9711 1.0000 1.0000 proteinBik , a novel death-inducing protein shares a distinct sequence motif with Bcl-2 family proteins and interacts with viral and cellular survival-promoting proteins .
Bik , a novel death-inducing protein shares a distinct sequence motif with Bcl-2 family proteins and interacts with viral and proteincellular survival-promoting proteins .
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2.1060 20.9933 0.9999 The survival-promoting activity of the Bcl-2 family of proteins appears to be modulated by interactions between various proteincellular proteins .
4.6540 30.2105 10.8013 The survival-promoting activity of the proteinBcl-2 family of proteins appears to be modulated by interactions between various cellular proteins .
The survival-promoting activity of the proteinBcl-2 family of proteins appears to be modulated by interactions between various cellular proteins .
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4.1504 20.9343 10.8040 We have identified a novel cellular protein , Bik , that interacts with the proteincellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
4.0278 20.6207 10.6811 We have identified a novel cellular protein , Bik , that interacts with the cellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the proteinviral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
3.6486 20.2807 10.5188 We have identified a novel cellular protein , Bik , that interacts with the cellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and proteinadenovirus E1B-19 kDa .
3.2059 10.8608 10.9927 We have identified a novel cellular protein , Bik , that interacts with the cellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , proteinEpstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
1.1361 0.9999 10.3248 We have identified a novel proteincellular protein , Bik , that interacts with the cellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
0.9674 1.0000 1.0000 We have identified a novel cellular protein , Bik , that interacts with the cellular survival-promoting proteins , Bcl-2 and proteinBcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
0.9661 1.0000 1.0000 We have identified a novel cellular protein , Bik , that interacts with the cellular survival-promoting proteins , proteinBcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
0.9280 1.0000 1.0000 We have identified a novel cellular protein , proteinBik , that interacts with the cellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
3.9732 20.8471 10.8274 We have identified a proteinnovel cellular protein , Bik , that interacts with the cellular survival-promoting proteins , Bcl-2 and Bcl-xL , as well as the viral survival-promoting proteins , Epstein Barr virus -BHRF1 and adenovirus E1B-19 kDa .
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2.1223 20.1229 1.0000 In transient transfection assays , Bik promotes cell death in a manner similar to the death-promoting members of the proteinBcl-2 family , Bax and Bak .
2.0164 20.8209 0.9999 In transient transfection assays , Bik promotes cell death in a manner similar to the proteindeath-promoting members of the Bcl-2 family , Bax and Bak .
1.9245 20.3601 0.9825 In transient transfection assays , Bik promotes cell death in a manner similar to the death-promoting members of the proteinBcl-2 family , Bax and Bak .
1.5471 10.8954 1.0000 In transient transfection assays , proteinBik promotes cell death in a manner similar to the death-promoting members of the Bcl-2 family , Bax and Bak .
0.9260 1.0000 1.0000 In transient transfection assays , Bik promotes cell death in a manner similar to the death-promoting members of the Bcl-2 family , proteinBax and Bak .
0.9159 1.0000 1.0000 In transient transfection assays , Bik promotes cell death in a manner similar to the death-promoting members of the Bcl-2 family , Bax and proteinBak .
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1.5234 10.4222 1.0000 This death-promoting activity of proteinBik can be suppressed by coexpression of Bcl-2 , Bcl-XL , EBV-BHRF1 and E1B-19 kDa proteins suggesting that Bik may be a common target for both cellular and viral anti-apoptotic proteins .
0.9669 1.0000 1.0000 This death-promoting activity of Bik can be suppressed by coexpression of Bcl-2 , proteinBcl-XL , EBV-BHRF1 and E1B-19 kDa proteins suggesting that Bik may be a common target for both cellular and viral anti-apoptotic proteins .
0.9143 0.9999 1.0000 This death-promoting activity of Bik can be suppressed by coexpression of Bcl-2 , Bcl-XL , proteinEBV-BHRF1 and E1B-19 kDa proteins suggesting that Bik may be a common target for both cellular and viral anti-apoptotic proteins .
0.8919 1.0000 1.0000 This death-promoting activity of Bik can be suppressed by coexpression of proteinBcl-2 , Bcl-XL , EBV-BHRF1 and E1B-19 kDa proteins suggesting that Bik may be a common target for both cellular and viral anti-apoptotic proteins .
0.8401 1.0000 1.0000 This death-promoting activity of Bik can be suppressed by coexpression of Bcl-2 , Bcl-XL , EBV-BHRF1 and E1B-19 kDa proteins suggesting that proteinBik may be a common target for both cellular and viral anti-apoptotic proteins .
3.1624 10.8382 10.7481 This death-promoting activity of Bik can be suppressed by coexpression of Bcl-2 , Bcl-XL , EBV-BHRF1 and proteinE1B-19 kDa proteins suggesting that Bik may be a common target for both cellular and viral anti-apoptotic proteins .
This death-promoting activity of Bik can be suppressed by coexpression of Bcl-2 , Bcl-XL , EBV-BHRF1 and proteinE1B-19 kDa proteins suggesting that Bik may be a common target for both cellular and viral anti-apoptotic proteins .
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2.1624 20.1801 1.0000 While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the proteinBcl-2 family , it does share a 9 amino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
0.9606 1.0000 1.0000 While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 amino acid domain ( proteinBH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
0.9161 1.0000 1.0000 While proteinBik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 amino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
0.9025 1.0000 1.0000 While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 amino acid domain ( BH3 ) with Bax and proteinBak which may be a critical determinant for the death-promoting activity of these proteins.
0.8795 1.0000 1.0000 While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 amino acid domain ( BH3 ) with proteinBax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
0.7276 1.0000 1.0000 While Bik does not show overt homology to the proteinBH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 amino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
0.6597 1.0000 1.0000 While Bik does not show overt homology to the BH1 and proteinBH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 amino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
4.7532 20.9476 10.7372 While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a protein9 amino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
2.0487 20.6624 0.9912 While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the proteinBcl-2 family , it does share a 9 amino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
While Bik does not show overt homology to the BH1 and BH2 conserved domains characteristic of the Bcl-2 family , it does share a 9 proteinamino acid domain ( BH3 ) with Bax and Bak which may be a critical determinant for the death-promoting activity of these proteins.
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1.9589 30.0977 10.2108 The human TCF-1 gene encodes a proteinnuclear DNA-binding protein uniquely expressed in normal and neoplastic T-lineage lymphocytes .
0.6835 0.8590 0.9972 The DNAhuman TCF-1 gene encodes a nuclear DNA-binding protein uniquely expressed in normal and neoplastic T-lineage lymphocytes .
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2.1895 20.8410 0.9999 The TCF-1 gene encodes a putative transcription factor with affinity for a sequence motif occurring in a number of DNAT-cell enhancers .
2.0365 20.3352 0.9999 The TCF-1 gene encodes a putative transcription factor with affinity for a DNAsequence motif occurring in a number of T-cell enhancers .
1.5868 10.7079 0.9999 The DNATCF-1 gene encodes a putative transcription factor with affinity for a sequence motif occurring in a number of T-cell enhancers .
2.1912 20.1660 1.0000 The TCF-1 gene encodes a putative proteintranscription factor with affinity for a sequence motif occurring in a number of T-cell enhancers .
The proteinTCF-1 gene encodes a putative transcription factor with affinity for a sequence motif occurring in a number of T-cell enhancers .
The TCF-1 gene encodes a proteinputative transcription factor with affinity for a sequence motif occurring in a number of T-cell enhancers .
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0.9477 0.9985 1.0000 RNATCF-1 mRNA was originally found to be expressed in a T cell-specific fashion within a set of human and mouse cell lines .
0.9306 1.0000 0.9906 proteinTCF-1 mRNA was originally found to be expressed in a T cell-specific fashion within a set of human and mouse cell lines .
TCF-1 mRNA was originally found to be expressed in a T cell-specific fashion within a set of cell_linehuman and mouse cell lines .
TCF-1 mRNA was originally found to be expressed in a T cell-specific fashion within a set of cell_linehuman and mouse cell lines .
TCF-1 mRNA was originally found to be expressed in a T cell-specific fashion within a set of human and cell_linemouse cell lines .
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3.1292 20.8068 10.0944 We have now raised a monoclonal antibody to document expression and biochemistry of the proteinhuman TCF-1 protein .
2.1913 20.1097 1.0000 We have now raised a proteinmonoclonal antibody to document expression and biochemistry of the human TCF-1 protein .
We have now raised a monoclonal antibody to document expression and biochemistry of the human proteinTCF-1 protein .
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2.0695 20.7386 1.0000 As expected, the proteinTCF-1 protein was detectable only in cell lines of T lineage .
2.0341 20.3485 0.9984 As expected, the TCF-1 protein was detectable only in cell_linecell lines of T lineage .
1.7098 20.9085 0.9857 As expected, the proteinTCF-1 protein was detectable only in cell lines of T lineage .
0.8428 0.9938 0.9997 As expected, the TCF-1 protein was detectable only in cell lines of cell_typeT lineage .
As expected, the TCF-1 protein was detectable only in cell_linecell lines of T lineage .
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Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0193 20.8517 1.0000 Immunohistochemistry on a panel of human tissues revealed that the proteinTCF-1 protein was found exclusively in thymocytes and in CD3+ T cells in peripheral lymphoid tissues .
1.8771 20.7678 0.9939 Immunohistochemistry on a panel of human tissues revealed that the proteinTCF-1 protein was found exclusively in thymocytes and in CD3+ T cells in peripheral lymphoid tissues .
4.6566 20.9800 10.7738 Immunohistochemistry on a panel of human tissues revealed that the TCF-1 protein was found exclusively in thymocytes and in cell_typeCD3+ T cells in peripheral lymphoid tissues .
1.6178 10.4796 1.0000 Immunohistochemistry on a panel of human tissues revealed that the TCF-1 protein was found exclusively in cell_typethymocytes and in CD3+ T cells in peripheral lymphoid tissues .
Immunohistochemistry on a panel of human tissues revealed that the TCF-1 protein was found exclusively in thymocytes and in CD3+ cell_typeT cells in peripheral lymphoid tissues .
Immunohistochemistry on a panel of human tissues revealed that the TCF-1 protein was found exclusively in thymocytes and in cell_lineCD3+ T cells in peripheral lymphoid tissues .
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1.5214 10.7765 0.9999 Western blotting yielded a set of bands ranging from protein25 kD to 55 kD, resulting from extensive alternative splicing .
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2.3283 20.6284 0.9999 The TCF-1 protein was detectable in all samples of a set of 22 T-cell malignancies of various stages of maturation, but was absent from a large number of other cell_typehematologic neoplasms .
1.6548 10.9829 0.9928 The proteinTCF-1 protein was detectable in all samples of a set of 22 T-cell malignancies of various stages of maturation, but was absent from a large number of other hematologic neoplasms .
1.6880 10.5345 1.0000 The proteinTCF-1 protein was detectable in all samples of a set of 22 T-cell malignancies of various stages of maturation, but was absent from a large number of other hematologic neoplasms .
The TCF-1 protein was detectable in all samples of a set of 22 cell_typeT-cell malignancies of various stages of maturation, but was absent from a large number of other hematologic neoplasms .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6630 10.9237 1.0000 These observations imply a T cell-specific function for proteinTCF-1 , a notion corroborated by recent observations on Tcf-1 knock-out mice .
1.6492 10.2290 1.0000 These observations imply a T cell-specific function for TCF-1 , a notion corroborated by recent observations on proteinTcf-1 knock-out mice .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6987 10.9045 1.0000 In addition, these results indicate that nuclear proteinTCF-1 expression can serve as a pan-T-lineage marker in the diagnosis of lymphoid malignancies .
1.9106 20.0375 1.0000 In addition, these results indicate that nuclear TCF-1 expression can serve as a proteinpan-T-lineage marker in the diagnosis of lymphoid malignancies .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8490 20.5259 10.7077 Cross-linking of Fc gamma receptors activates DNAHIV-1 long terminal repeat -driven transcription in human monocytes .
3.8272 20.2125 10.9123 Cross-linking of proteinFc gamma receptors activates HIV-1 long terminal repeat -driven transcription in human monocytes .
1.8419 20.3505 0.9992 Cross-linking of Fc gamma receptors activates HIV-1 long terminal repeat -driven transcription in cell_typehuman monocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9362 20.6216 10.3727 Elevation of the levels of proteincirculating immune complexes frequently accompanies HIV-1 infection and is a prognostic indicator of clinical progression from asymptomatic infection to AIDS .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9565 20.8556 10.6523 Here we report that cross-linking of proteinFc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
2.7650 10.8027 10.7201 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by proteinadherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
2.2795 20.6136 0.9998 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific proteinanti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
2.1443 20.4415 0.9999 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased RNAHIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
2.1328 10.9904 10.3229 Here we report that cross-linking of Fc gamma RI or proteinFc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
0.8660 1.0000 1.0000 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in cell_typemonocytes from HIV infected patients as assayed by reverse transcription-PCR .
6.2879 30.5945 10.9094 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the cell_linehuman monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
1.4826 20.4193 0.4318 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific proteinanti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
0.6652 0.9924 0.9998 Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates DNAHIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the human monocytic cell line cell_lineBF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
Here we report that cross-linking of Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R mAb activates HIV-1 gene expression in the cell_linehuman monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8923 20.4587 10.3038 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the DNAlong terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
2.3326 30.3233 0.9999 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not proteinanti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
2.2171 10.9701 10.0822 In cell_lineTHP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
2.1786 20.5744 1.0000 In THP-1 cells , Fc gamma R cross-linking induced proteinNF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
2.1588 20.7887 0.9999 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of proteinNF-kappa B by Fc gamma R cross-linking .
2.0504 20.7888 0.9999 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the DNAregulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
1.4622 10.0426 0.9992 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by proteinFc gamma R cross-linking .
0.9503 1.0000 1.0000 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( DNALTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
0.9056 1.0000 1.0000 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - DNALTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
0.7308 0.9835 0.9985 In THP-1 cells , proteinFc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
0.7224 0.9906 0.9998 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . proteinAnti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
1.9845 30.2548 10.7813 In THP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of DNAHIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
In cell_lineTHP-1 cells , Fc gamma R cross-linking induced NF-kappa B , which is known to bind to the regulatory region of the long terminal repeat ( LTR ) of HIV-1 and to activate HIV-1 transcription . Anti-TNF-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1 - LTR -driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5696 20.5186 10.9248 These results indicate that proteinFc gamma R can mediate a TNF-alpha -dependent induction of HIV-1 gene transcription and suggest that immune complexes may contribute to the pathophysiology of HIV-1 infection by augmenting viral replication in monocytes .
1.6000 10.0142 1.0000 These results indicate that Fc gamma R can mediate a TNF-alpha -dependent induction of HIV-1 gene transcription and suggest that immune complexes may contribute to the pathophysiology of HIV-1 infection by augmenting viral replication in cell_typemonocytes .
1.4482 10.3118 0.9999 These results indicate that Fc gamma R can mediate a TNF-alpha -dependent induction of HIV-1 gene transcription and suggest that proteinimmune complexes may contribute to the pathophysiology of HIV-1 infection by augmenting viral replication in monocytes .
1.3101 10.0126 0.9999 These results indicate that Fc gamma R can mediate a TNF-alpha -dependent induction of DNAHIV-1 gene transcription and suggest that immune complexes may contribute to the pathophysiology of HIV-1 infection by augmenting viral replication in monocytes .
0.9082 1.0000 1.0000 These results indicate that Fc gamma R can mediate a proteinTNF-alpha -dependent induction of HIV-1 gene transcription and suggest that immune complexes may contribute to the pathophysiology of HIV-1 infection by augmenting viral replication in monocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.1301 10.5199 1.0000 Signalling via proteinCD28 of human naive neonatal T lymphocytes .
4.4342 20.7725 20.5284 Signalling via CD28 of cell_typehuman naive neonatal T lymphocytes .
Signalling via CD28 of cell_linehuman naive neonatal T lymphocytes .
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0.9256 0.9999 1.0000 proteinAccessory molecules play a crucial role in the development of the T cell response to antigenic challenge.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6245 10.5607 1.0000 We have examined the role of proteinCD28 in modulating the ' naive' neonatal T cell response to anti-CD2 -mediated activation .
0.9191 1.0000 1.0000 We have examined the role of CD28 in modulating the ' naive' neonatal T cell response to proteinanti-CD2 -mediated activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1595 20.8834 10.0277 To compare the role of CD28 , neonatal and adult T cells were stimulated with a pair of mitogenic anti-CD2 antibodies in the presence or absence of proteinanti- CD28 MoAb .
3.1282 20.2298 10.4164 To compare the role of CD28 , neonatal and adult T cells were stimulated with a pair of proteinmitogenic anti-CD2 antibodies in the presence or absence of anti- CD28 MoAb .
1.5740 10.4882 1.0000 To compare the role of proteinCD28 , neonatal and adult T cells were stimulated with a pair of mitogenic anti-CD2 antibodies in the presence or absence of anti- CD28 MoAb .
0.9204 1.0000 0.9872 To compare the role of CD28 , neonatal and adult T cells were stimulated with a pair of mitogenic anti-CD2 antibodies in the presence or absence of anti- proteinCD28 MoAb .
To compare the role of CD28 , neonatal and cell_typeadult T cells were stimulated with a pair of mitogenic anti-CD2 antibodies in the presence or absence of anti- CD28 MoAb .
To compare the role of CD28 , cell_typeneonatal and adult T cells were stimulated with a pair of mitogenic anti-CD2 antibodies in the presence or absence of anti- CD28 MoAb .
To compare the role of CD28 , neonatal and adult cell_typeT cells were stimulated with a pair of mitogenic anti-CD2 antibodies in the presence or absence of anti- CD28 MoAb .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6205 20.8471 10.8259 With anti-CD2 alone, cell_typeneonatal T cells proliferated slightly but produced no detectable IL-2 , whereas adult T cells proliferated vigorously, with significant IL-2 production .
1.6202 10.2405 1.0000 With proteinanti-CD2 alone, neonatal T cells proliferated slightly but produced no detectable IL-2 , whereas adult T cells proliferated vigorously, with significant IL-2 production .
1.5740 10.1523 1.0000 With anti-CD2 alone, neonatal T cells proliferated slightly but produced no detectable IL-2 , whereas adult T cells proliferated vigorously, with significant proteinIL-2 production .
1.4452 10.9707 1.0000 With anti-CD2 alone, neonatal T cells proliferated slightly but produced no detectable proteinIL-2 , whereas adult T cells proliferated vigorously, with significant IL-2 production .
4.2245 20.6159 10.8107 With anti-CD2 alone, neonatal T cells proliferated slightly but produced no detectable IL-2 , whereas cell_typeadult T cells proliferated vigorously, with significant IL-2 production .
With anti-CD2 alone, neonatal T cells proliferated slightly but produced no detectable IL-2 , whereas adult cell_typeT cells proliferated vigorously, with significant IL-2 production .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9950 20.9266 10.9039 Costimulation with anti- CD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of adult T cells , whereas cell_typeadult T cells showed only slight increases.
3.9360 20.9251 10.8672 Costimulation with anti- CD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of cell_typeadult T cells , whereas adult T cells showed only slight increases.
3.3090 20.5459 10.9629 Costimulation with anti- CD28 MoAb greatly enhanced the proliferative response of cell_typeneonatal T cells to levels equivalent to those of adult T cells , whereas adult T cells showed only slight increases.
2.2710 20.9004 10.2605 Costimulation with proteinanti- CD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of adult T cells , whereas adult T cells showed only slight increases.
1.8151 20.5072 0.9856 Costimulation with anti- proteinCD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of adult T cells , whereas adult T cells showed only slight increases.
Costimulation with anti- CD28 MoAb greatly enhanced the proliferative response of neonatal cell_typeT cells to levels equivalent to those of adult T cells , whereas adult T cells showed only slight increases.
Costimulation with anti- CD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of adult T cells , whereas adult cell_typeT cells showed only slight increases.
Costimulation with anti- CD28 MoAb greatly enhanced the proliferative response of neonatal T cells to levels equivalent to those of adult cell_typeT cells , whereas adult T cells showed only slight increases.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9916 20.7616 10.4792 Although IL-2 secretion was increased in the presence of proteinanti- CD28 MoAb , neonatal T cell IL-2 production remained lower than in adults .
2.7824 10.3885 10.4959 Although IL-2 secretion was increased in the presence of anti- CD28 MoAb , cell_typeneonatal T cell IL-2 production remained lower than in adults .
0.9583 1.0000 0.9999 Although IL-2 secretion was increased in the presence of anti- CD28 MoAb , neonatal T cell proteinIL-2 production remained lower than in adults .
0.9396 1.0000 1.0000 Although proteinIL-2 secretion was increased in the presence of anti- CD28 MoAb , neonatal T cell IL-2 production remained lower than in adults .
0.9000 1.0000 0.9731 Although IL-2 secretion was increased in the presence of anti- proteinCD28 MoAb , neonatal T cell IL-2 production remained lower than in adults .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0685 20.0866 0.9940 In contrast, enhancement of proteinIL-2 mRNA expression in neonates was similar to adult levels .
1.6841 10.8504 1.0000 In contrast, enhancement of RNAIL-2 mRNA expression in neonates was similar to adult levels .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5761 20.2877 10.8888 Anti- CD28 MoAb costimulation increased proteinNF kappa B levels in neonates , albeit to levels lower than that of adults .
0.9503 1.0000 0.9755 Anti- proteinCD28 MoAb costimulation increased NF kappa B levels in neonates , albeit to levels lower than that of adults .
0.8283 0.9905 0.9997 proteinAnti- CD28 MoAb costimulation increased NF kappa B levels in neonates , albeit to levels lower than that of adults .
0.4646 0.9994 0.5364 proteinAnti- CD28 MoAb costimulation increased NF kappa B levels in neonates , albeit to levels lower than that of adults .
Anti- proteinCD28 MoAb costimulation increased NF kappa B levels in neonates , albeit to levels lower than that of adults .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6198 20.3086 10.6316 The cellular mechanism governing the diminished proliferative response of neonatal T lymphocytes to anti-CD2 may therefore be due to decreased proteinNF kappa B induction , reduced IL-2 mRNA expression and deficient IL-2 production .
3.5498 20.6067 10.6004 The cellular mechanism governing the diminished proliferative response of cell_typeneonatal T lymphocytes to anti-CD2 may therefore be due to decreased NF kappa B induction , reduced IL-2 mRNA expression and deficient IL-2 production .
2.0238 20.0052 0.9912 The cellular mechanism governing the diminished proliferative response of neonatal T lymphocytes to anti-CD2 may therefore be due to decreased NF kappa B induction , reduced proteinIL-2 mRNA expression and deficient IL-2 production .
1.4243 10.7612 1.0000 The cellular mechanism governing the diminished proliferative response of neonatal T lymphocytes to anti-CD2 may therefore be due to decreased NF kappa B induction , reduced RNAIL-2 mRNA expression and deficient IL-2 production .
0.8559 1.0000 1.0000 The cellular mechanism governing the diminished proliferative response of neonatal T lymphocytes to proteinanti-CD2 may therefore be due to decreased NF kappa B induction , reduced IL-2 mRNA expression and deficient IL-2 production .
0.8354 1.0000 1.0000 The cellular mechanism governing the diminished proliferative response of neonatal T lymphocytes to anti-CD2 may therefore be due to decreased NF kappa B induction , reduced IL-2 mRNA expression and deficient proteinIL-2 production .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1855 10.6888 10.5775 Although proteinanti- CD28 MoAb costimulation enhances all of the above signals, NF kappa B and IL-2 levels remain lower than in adults , suggesting the need for further activation requirements in the neonate .
0.9601 1.0000 0.9854 Although anti- proteinCD28 MoAb costimulation enhances all of the above signals, NF kappa B and IL-2 levels remain lower than in adults , suggesting the need for further activation requirements in the neonate .
3.7894 20.7987 10.8065 Although anti- CD28 MoAb costimulation enhances all of the above signals, proteinNF kappa B and IL-2 levels remain lower than in adults , suggesting the need for further activation requirements in the neonate .
0.9077 1.0000 1.0000 Although anti- CD28 MoAb costimulation enhances all of the above signals, NF kappa B and proteinIL-2 levels remain lower than in adults , suggesting the need for further activation requirements in the neonate .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4037 20.1058 10.5493 TCL1 oncogene activation in cell_typepreleukemic T cells from a case of ataxia-telangiectasia .
0.8428 0.9987 0.9999 DNATCL1 oncogene activation in preleukemic T cells from a case of ataxia-telangiectasia .
TCL1 oncogene activation in preleukemic cell_typeT cells from a case of ataxia-telangiectasia .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6281 20.0300 10.6804 The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with DNATCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
1.4931 10.4637 0.9999 The DNATCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
0.8545 1.0000 1.0000 The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and DNAt(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
0.8499 1.0000 1.0000 The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ DNAinv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
0.8295 0.9999 1.0000 The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [ DNAt(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
2.3543 10.7073 10.9608 The TCL1 oncogene on DNAhuman chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
0.8153 1.0000 1.0000 The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and DNAinversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
0.5904 0.9946 1.0000 The TCL1 oncogene on human chromosome 14q32.1 is involved in DNAchromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
The TCL1 oncogene on DNAhuman chromosome 14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
The TCL1 oncogene on human chromosome DNA14q32.1 is involved in chromosome translocations [ t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1) ] and inversions [ inv14(q11;q32.1) ] with TCR alpha/beta loci in T-cell leukemias , such as T-prolymphocytic ( T-PLL ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7136 10.3913 0.9999 Similar chromosomal rearrangements occur also in the clonally expanded cell_typeT cells in AT patients before the appearance of the overt leukemia .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0217 10.9434 10.8882 We have analyzed the expression of TCL1 mRNA and protein in cell_typeperipheral blood lymphocytes ( PBLs ) from four AT cases and from healthy controls .
2.4974 20.1523 1.0000 We have analyzed the expression of RNATCL1 mRNA and protein in peripheral blood lymphocytes ( PBLs ) from four AT cases and from healthy controls .
0.9484 1.0000 1.0000 We have analyzed the expression of TCL1 mRNA and protein in peripheral blood lymphocytes ( cell_typePBLs ) from four AT cases and from healthy controls .
2.0811 20.2596 0.9928 We have analyzed the expression of proteinTCL1 mRNA and protein in peripheral blood lymphocytes ( PBLs ) from four AT cases and from healthy controls .
We have analyzed the expression of TCL1 mRNA and proteinprotein in peripheral blood lymphocytes ( PBLs ) from four AT cases and from healthy controls .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1060 20.8849 1.0000 We found that the DNATCL1 gene was overexpressed in the PBLs of an AT patient with a large clonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases.
1.6869 10.1412 1.0000 We found that the TCL1 gene was overexpressed in the PBLs of an AT patient with a large clonal T-cell population exhibiting the t(14;14) translocation but not in the cell_typelymphocytes of the other cases.
1.6792 10.4845 1.0000 We found that the TCL1 gene was overexpressed in the cell_typePBLs of an AT patient with a large clonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases.
2.8879 20.5782 10.6149 We found that the TCL1 gene was overexpressed in the PBLs of an AT patient with a large cell_typeclonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases.
2.1176 20.3869 0.9999 We found that the TCL1 gene was overexpressed in the PBLs of an AT patient with a large clonal T-cell population exhibiting the DNAt(14;14) translocation but not in the lymphocytes of the other cases.
1.9679 20.9319 0.9910 We found that the proteinTCL1 gene was overexpressed in the PBLs of an AT patient with a large clonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases.
We found that the TCL1 gene was overexpressed in the PBLs of an AT patient with a cell_linelarge clonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5990 30.3097 10.5166 Fluorescence in situ hybridization of the DNATCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the distal part of chromosome 14 .
2.2292 20.4667 1.0000 Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the DNATCL1 locus and is accompanied by an inverted duplication of the distal part of chromosome 14 .
0.8712 0.9982 0.9998 Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the distal part of DNAchromosome 14 .
3.1400 30.2661 10.0006 Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the DNAdistal part of chromosome 14 .
2.2047 20.9610 0.9999 Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the DNAt(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the distal part of chromosome 14 .
Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an DNAinverted duplication of the distal part of chromosome 14 .
Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the DNAdistal part of chromosome 14 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.0529 20.3074 0.9999 These data indicate that TCL1 is activated in preleukemic clonal cells as a consequence of chromosome translocation involving sequences from the DNATCR locus at 14q11 .
0.9167 1.0000 1.0000 These data indicate that TCL1 is activated in preleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at DNA14q11 .
3.5523 20.3015 10.6508 These data indicate that TCL1 is activated in cell_typepreleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at 14q11 .
1.5239 10.6910 1.0000 These data indicate that proteinTCL1 is activated in preleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at 14q11 .
These data indicate that DNATCL1 is activated in preleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at 14q11 .
These data indicate that TCL1 is activated in cell_linepreleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at 14q11 .
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1.7669 10.7941 1.0000 Deregulation of proteinTCL1 is the first event in the initiation of malignancy in these types of leukemias and represents a potential tool for clinical evaluation .
Deregulation of DNATCL1 is the first event in the initiation of malignancy in these types of leukemias and represents a potential tool for clinical evaluation .
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6.3410 30.7956 20.6807 C/EBP proteins activate transcription from the DNAhuman immunodeficiency virus type 1 long terminal repeat in macrophages/ monocytes .
0.8921 1.0000 0.9999 C/EBP proteins activate transcription from the human immunodeficiency virus type 1 long terminal repeat in macrophages/ cell_typemonocytes .
0.8011 0.9998 0.9999 proteinC/EBP proteins activate transcription from the human immunodeficiency virus type 1 long terminal repeat in macrophages/ monocytes .
1.4564 10.5825 0.9995 C/EBP proteins activate transcription from the human immunodeficiency virus type 1 long terminal repeat in cell_typemacrophages/ monocytes .
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3.2203 10.2391 20.6367 Three binding sites for C/EBP proteins are found in the DNAhuman immunodeficiency virus type 1 ( HIV-1 ) long terminal repeat ( LTR ) (V.M. Tesmer, A.Rajadhyaksha, J.Babin, and M.Bina, Proc.Natl.Acad.Sci. USA 90:7298-7302, 1993).
1.3891 10.6204 1.0000 Three binding sites for proteinC/EBP proteins are found in the human immunodeficiency virus type 1 ( HIV-1 ) long terminal repeat ( LTR ) (V.M. Tesmer, A.Rajadhyaksha, J.Babin, and M.Bina, Proc.Natl.Acad.Sci. USA 90:7298-7302, 1993).
0.9511 0.9999 1.0000 Three binding sites for C/EBP proteins are found in the human immunodeficiency virus type 1 ( HIV-1 ) long terminal repeat ( DNALTR ) (V.M. Tesmer, A.Rajadhyaksha, J.Babin, and M.Bina, Proc.Natl.Acad.Sci. USA 90:7298-7302, 1993).
1.2664 10.0766 0.9999 Three DNAbinding sites for C/EBP proteins are found in the human immunodeficiency virus type 1 ( HIV-1 ) long terminal repeat ( LTR ) (V.M. Tesmer, A.Rajadhyaksha, J.Babin, and M.Bina, Proc.Natl.Acad.Sci. USA 90:7298-7302, 1993).
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3.0882 20.7166 10.5902 We have determined the functional role of C/EBP proteins and C/EBP sites in regulating transcription from the DNAHIV- 1 LTR in monocytes /macrophages .
2.1685 20.5603 1.0000 We have determined the functional role of proteinC/EBP proteins and C/EBP sites in regulating transcription from the HIV- 1 LTR in monocytes /macrophages .
1.6598 10.7212 0.9998 We have determined the functional role of C/EBP proteins and C/EBP sites in regulating transcription from the HIV- 1 LTR in cell_typemonocytes /macrophages .
1.5489 10.8268 0.9999 We have determined the functional role of C/EBP proteins and DNAC/EBP sites in regulating transcription from the HIV- 1 LTR in monocytes /macrophages .
1.5330 10.8885 0.9762 We have determined the functional role of C/EBP proteins and C/EBP sites in regulating transcription from the HIV- 1 LTR in cell_typemonocytes /macrophages .
0.7909 1.0000 0.9998 We have determined the functional role of C/EBP proteins and C/EBP sites in regulating transcription from the HIV- 1 LTR in monocytes cell_type/macrophages .
0.5110 0.9999 0.9994 We have determined the functional role of C/EBP proteins and C/EBP sites in regulating transcription from the HIV- DNA1 LTR in monocytes /macrophages .
We have determined the functional role of C/EBP proteins and C/EBP sites in regulating transcription from the HIV- 1 DNALTR in monocytes /macrophages .
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4.8230 20.5894 10.9193 Inhibition of endogenous C/EBP proteins , using either an excess of C/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of HIV-1 LTR transcription in the cell_linepromonocytic cell line U937 .
3.5942 20.5352 10.6011 Inhibition of endogenous C/EBP proteins , using either an excess of DNAC/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of HIV-1 LTR transcription in the promonocytic cell line U937 .
2.6286 20.6935 10.4441 Inhibition of proteinendogenous C/EBP proteins , using either an excess of C/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of HIV-1 LTR transcription in the promonocytic cell line U937 .
2.0999 20.7844 0.9999 Inhibition of endogenous C/EBP proteins , using either an excess of C/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of DNAHIV-1 LTR transcription in the promonocytic cell line U937 .
1.4713 20.0988 10.2876 Inhibition of endogenous proteinC/EBP proteins , using either an excess of C/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of HIV-1 LTR transcription in the promonocytic cell line U937 .
1.4624 10.8494 1.0000 Inhibition of endogenous C/EBP proteins , using either an excess of C/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that proteinC/EBP proteins are required for basal and activated levels of HIV-1 LTR transcription in the promonocytic cell line U937 .
Inhibition of endogenous C/EBP proteins , using either an excess of C/EBP binding sites or a trans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of HIV-1 DNALTR transcription in the promonocytic cell line U937 .
Inhibition of endogenous C/EBP proteins , using either an excess of C/EBP binding sites or a DNAtrans- dominant negative inhibitor , demonstrated that C/EBP proteins are required for basal and activated levels of HIV-1 LTR transcription in the promonocytic cell line U937 .
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2.3272 20.4828 0.9999 Northern (RNA) blots and binding assays showed that NF-IL6 is the only known proteinC/EBP family member which is increased when U937 cells are activated.
2.3026 20.0753 0.9999 Northern (RNA) blots and binding assays showed that NF-IL6 is the only known C/EBP family member which is increased when cell_lineU937 cells are activated.
1.7439 10.1159 1.0000 Northern (RNA) blots and binding assays showed that proteinNF-IL6 is the only known C/EBP family member which is increased when U937 cells are activated.
1.7927 20.6283 0.7600 Northern (RNA) blots and binding assays showed that NF-IL6 is the only known proteinC/EBP family member which is increased when U937 cells are activated.
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2.2800 20.2648 1.0000 Mutational analyses of the DNAHIV-1 LTR showed that one C/EBP site is required for normal LTR transcription both before and after cellular activation and that the two 3' C/EBP sites are functionally equivalent.
1.5341 10.9706 1.0000 Mutational analyses of the HIV-1 LTR showed that one DNAC/EBP site is required for normal LTR transcription both before and after cellular activation and that the two 3' C/EBP sites are functionally equivalent.
0.8583 0.9999 1.0000 Mutational analyses of the HIV-1 LTR showed that one C/EBP site is required for normal DNALTR transcription both before and after cellular activation and that the two 3' C/EBP sites are functionally equivalent.
3.9240 20.8831 10.9958 Mutational analyses of the HIV-1 LTR showed that one C/EBP site is required for normal LTR transcription both before and after cellular activation and that the two DNA3' C/EBP sites are functionally equivalent.
Mutational analyses of the HIV-1 DNALTR showed that one C/EBP site is required for normal LTR transcription both before and after cellular activation and that the two 3' C/EBP sites are functionally equivalent.
Mutational analyses of the HIV-1 LTR showed that one C/EBP site is required for normal LTR transcription both before and after cellular activation and that the two 3' DNAC/EBP sites are functionally equivalent.
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2.2770 20.2658 0.9999 However, transcription from crippled HIV-1 LTRs lacking C/EBP sites can still be induced following activation of cell_lineU937 cells .
1.5404 10.6795 0.9998 However, transcription from crippled HIV-1 LTRs lacking DNAC/EBP sites can still be induced following activation of U937 cells .
2.3804 20.0077 0.9999 However, transcription from crippled DNAHIV-1 LTRs lacking C/EBP sites can still be induced following activation of U937 cells .
However, transcription from crippled HIV-1 DNALTRs lacking C/EBP sites can still be induced following activation of U937 cells .
However, transcription from DNAcrippled HIV-1 LTRs lacking C/EBP sites can still be induced following activation of U937 cells .
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1.7786 10.2203 1.0000 Several models are suggested for how elevated NF-IL6 may participate in an autostimulatory loop involving HIV infection , macrophage activation , proteincytokine expression , and HIV replication .
1.7038 10.7505 1.0000 Several models are suggested for how elevated proteinNF-IL6 may participate in an autostimulatory loop involving HIV infection , macrophage activation , cytokine expression , and HIV replication .
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1.7506 10.3044 1.0000 Human immunodeficiency virus type-2 gene expression : two DNAenhancers and their activation by T-cell activators .
2.1295 20.6464 0.9999 Human immunodeficiency virus type-2 gene expression : two enhancers and their activation by proteinT-cell activators .
Human immunodeficiency virus type-2 gene expression : two enhancers and their activation by cell_typeT-cell activators .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8288 20.7255 10.5542 Since expression of the viruses is in large part regulated by the sequence elements in their DNAlong terminal repeats ( LTRs ), this study was directed to an analysis of the regulatory elements in the HIV-2 LTR .
2.2422 20.5243 0.9999 Since expression of the viruses is in large part regulated by the sequence elements in their long terminal repeats ( LTRs ), this study was directed to an analysis of the regulatory elements in the DNAHIV-2 LTR .
2.1973 20.9094 0.9999 Since expression of the viruses is in large part regulated by the sequence elements in their long terminal repeats ( LTRs ), this study was directed to an analysis of the DNAregulatory elements in the HIV-2 LTR .
1.3781 10.8863 0.9999 Since expression of the viruses is in large part regulated by the DNAsequence elements in their long terminal repeats ( LTRs ), this study was directed to an analysis of the regulatory elements in the HIV-2 LTR .
0.9542 1.0000 1.0000 Since expression of the viruses is in large part regulated by the sequence elements in their long terminal repeats ( DNALTRs ), this study was directed to an analysis of the regulatory elements in the HIV-2 LTR .
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1.7044 10.0182 1.0000 The HIV-2 LTR was found to contain two DNAenhancers .
1.5371 10.6581 1.0000 The DNAHIV-2 LTR was found to contain two enhancers .
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2.2409 20.1892 0.9999 One of these enhancers is, in part, identical to the DNAHIV-1 enhancer .
1.7163 10.5607 0.9999 One of these DNAenhancers is, in part, identical to the HIV-1 enhancer .
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4.1599 20.8382 10.8746 This enhancer in HIV-1 is the DNAT-cell activation response element ; in HIV-2 , however, it is the second enhancer that is mainly responsible for activation in response to T-cell activators .
0.8747 0.9999 1.0000 This DNAenhancer in HIV-1 is the T-cell activation response element ; in HIV-2 , however, it is the second enhancer that is mainly responsible for activation in response to T-cell activators .
2.2102 20.8710 0.9999 This enhancer in HIV-1 is the T-cell activation response element ; in HIV-2 , however, it is the second enhancer that is mainly responsible for activation in response to proteinT-cell activators .
0.9028 1.0000 1.0000 This enhancer in HIV-1 is the T-cell activation response element ; in HIV-2 , however, it is the second DNAenhancer that is mainly responsible for activation in response to T-cell activators .
This enhancer in HIV-1 is the T-cell activation response element ; in HIV-2 , however, it is the DNAsecond enhancer that is mainly responsible for activation in response to T-cell activators .
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3.7103 20.3215 10.8533 The second enhancer interacts with two proteinnuclear binding proteins (85 kD and 27 kD mobility) that appear to be required for optimal enhancer function and activation.
0.9274 1.0000 1.0000 The second DNAenhancer interacts with two nuclear binding proteins (85 kD and 27 kD mobility) that appear to be required for optimal enhancer function and activation.
0.5866 0.9999 0.9999 The second enhancer interacts with two nuclear binding proteins (85 kD and 27 kD mobility) that appear to be required for optimal DNAenhancer function and activation.
Cls_Score Left_Reg_Score Right_Reg_Score Text
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4.4421 20.9012 10.8154 NF-M ( chicken C/EBP beta ) induces eosinophilic differentiation and apoptosis in a cell_linehematopoietic progenitor cell line .
2.7871 20.1928 10.4456 NF-M ( proteinchicken C/EBP beta ) induces eosinophilic differentiation and apoptosis in a hematopoietic progenitor cell line .
0.9565 1.0000 1.0000 proteinNF-M ( chicken C/EBP beta ) induces eosinophilic differentiation and apoptosis in a hematopoietic progenitor cell line .
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1.5496 0.9985 10.3579 proteinCAAT/enhancer binding proteins ( C/EBPs ) are transcriptional activators implicated in the differentiation processes of various cell lineages.
0.9744 1.0000 1.0000 CAAT/enhancer binding proteins ( proteinC/EBPs ) are transcriptional activators implicated in the differentiation processes of various cell lineages.
1.3691 10.7820 0.9999 CAAT/enhancer binding proteins ( C/EBPs ) are proteintranscriptional activators implicated in the differentiation processes of various cell lineages.
DNACAAT/enhancer binding proteins ( C/EBPs ) are transcriptional activators implicated in the differentiation processes of various cell lineages.
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1.6187 10.9194 1.0000 We have shown earlier that NF-M , the chicken homolog of proteinC/EBP beta , is specifically expressed in myelomonocytic and eosinophilic cells of the hematopoietic system.
0.9430 1.0000 1.0000 We have shown earlier that proteinNF-M , the chicken homolog of C/EBP beta , is specifically expressed in myelomonocytic and eosinophilic cells of the hematopoietic system.
We have shown earlier that NF-M , the proteinchicken homolog of C/EBP beta , is specifically expressed in myelomonocytic and eosinophilic cells of the hematopoietic system.
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3.5658 20.5978 10.7981 To investigate the role of NF-M in hematopoietic cell lineage commitment, we constructed a conditional form of the protein by fusing it to the proteinhormone binding domain of the human estrogen receptor .
3.5070 20.5118 10.9116 To investigate the role of NF-M in hematopoietic cell lineage commitment, we constructed a conditional form of the protein by fusing it to the hormone binding domain of the proteinhuman estrogen receptor .
1.4849 10.3554 1.0000 To investigate the role of proteinNF-M in hematopoietic cell lineage commitment, we constructed a conditional form of the protein by fusing it to the hormone binding domain of the human estrogen receptor .
2.8804 10.9400 10.6595 To investigate the role of NF-M in cell_typehematopoietic cell lineage commitment, we constructed a conditional form of the protein by fusing it to the hormone binding domain of the human estrogen receptor .
To investigate the role of NF-M in cell_linehematopoietic cell lineage commitment, we constructed a conditional form of the protein by fusing it to the hormone binding domain of the human estrogen receptor .
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3.9603 20.3572 10.7019 This construct was stably expressed in a cell_linemultipotent progenitor cell line transformed by the Myb-Ets oncoprotein .
1.9461 20.0867 0.9999 This construct was stably expressed in a multipotent progenitor cell line transformed by the proteinMyb-Ets oncoprotein .
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3.8449 30.6074 10.4929 We report here that both NF-M -dependent promoter constructs and resident genes could be activated by addition of beta-estradiol to the cell_lineNF-M -estrogen receptor expressing progenitors .
3.7583 20.9861 10.4425 We report here that both DNANF-M -dependent promoter constructs and resident genes could be activated by addition of beta-estradiol to the NF-M -estrogen receptor expressing progenitors .
1.9064 20.5014 0.9964 We report here that both proteinNF-M -dependent promoter constructs and resident genes could be activated by addition of beta-estradiol to the NF-M -estrogen receptor expressing progenitors .
1.2744 20.4724 0.9982 We report here that both NF-M -dependent promoter constructs and resident genes could be activated by addition of beta-estradiol to the proteinNF-M -estrogen receptor expressing progenitors .
1.3322 10.5531 0.9997 We report here that both NF-M -dependent promoter constructs and DNAresident genes could be activated by addition of beta-estradiol to the NF-M -estrogen receptor expressing progenitors .
We report here that both NF-M -dependent promoter constructs and resident genes could be activated by addition of beta-estradiol to the proteinNF-M -estrogen receptor expressing progenitors .
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3.9446 20.6766 10.4322 At the same time, we observed a down-regulation of proteinprogenitor-specific surface markers and the up-regulation of differentiation markers restricted to the eosinophil and myeloid lineages .
1.5272 10.9978 1.0000 At the same time, we observed a down-regulation of progenitor-specific surface markers and the up-regulation of proteindifferentiation markers restricted to the eosinophil and myeloid lineages .
At the same time, we observed a down-regulation of progenitor-specific surface markers and the up-regulation of differentiation markers restricted to the cell_typeeosinophil and myeloid lineages .
At the same time, we observed a down-regulation of progenitor-specific surface markers and the up-regulation of differentiation markers restricted to the eosinophil and cell_typemyeloid lineages .
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2.3727 20.1851 1.0000 Our results suggest that NF-M plays an important role in commitment along the cell_typeeosinophil lineage and in the induction of apoptosis .
1.6201 10.7237 1.0000 Our results suggest that proteinNF-M plays an important role in commitment along the eosinophil lineage and in the induction of apoptosis .
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2.8454 20.6445 10.6975 Prolactin and interleukin-2 receptors in T lymphocytes signal through a proteinMGF-STAT5-like transcription factor .
1.3122 10.9192 0.9998 Prolactin and interleukin-2 receptors in cell_typeT lymphocytes signal through a MGF-STAT5-like transcription factor .
1.2401 10.5236 0.9999 Prolactin and proteininterleukin-2 receptors in T lymphocytes signal through a MGF-STAT5-like transcription factor .
proteinProlactin and interleukin-2 receptors in T lymphocytes signal through a MGF-STAT5-like transcription factor .
Prolactin and proteininterleukin-2 receptors in T lymphocytes signal through a MGF-STAT5-like transcription factor .
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2.1068 20.3510 0.9999 The cell surface receptors for PRL and interleukin-2 ( IL-2 ) are structurally distinct, but share regulatory tasks in cell_typeT lymphocytes .
0.9802 1.0000 1.0000 The cell surface receptors for PRL and interleukin-2 ( proteinIL-2 ) are structurally distinct, but share regulatory tasks in T lymphocytes .
0.9310 1.0000 1.0000 The cell surface receptors for proteinPRL and interleukin-2 ( IL-2 ) are structurally distinct, but share regulatory tasks in T lymphocytes .
0.9126 1.0000 1.0000 The cell surface receptors for PRL and proteininterleukin-2 ( IL-2 ) are structurally distinct, but share regulatory tasks in T lymphocytes .
3.0055 10.8709 10.6211 The proteincell surface receptors for PRL and interleukin-2 ( IL-2 ) are structurally distinct, but share regulatory tasks in T lymphocytes .
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1.6263 10.6210 0.9998 They can stimulate proliferation and activate transcription of over-lapping sets of genes of cell_typeT cells .
0.6415 0.9996 1.0000 They can stimulate proliferation and activate transcription of over-lapping sets of DNAgenes of T cells .
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7.2153 30.6014 20.9707 PRL and IL-2 receptor activation are both linked to the Jak/Stat ( proteinsignal transducer and activator of transcription ) pathway .
1.5752 10.4348 1.0000 PRL and IL-2 receptor activation are both linked to the proteinJak/Stat ( signal transducer and activator of transcription ) pathway .
0.8486 1.0000 1.0000 proteinPRL and IL-2 receptor activation are both linked to the Jak/Stat ( signal transducer and activator of transcription ) pathway .
0.7868 0.9999 1.0000 PRL and proteinIL-2 receptor activation are both linked to the Jak/Stat ( signal transducer and activator of transcription ) pathway .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.8434 10.7788 10.5447 We investigated the ability of PRL and IL-2 to activate Stat proteins in different cell_lineT cell lines .
1.6419 10.0969 1.0000 We investigated the ability of proteinPRL and IL-2 to activate Stat proteins in different T cell lines .
1.3381 10.7921 0.9999 We investigated the ability of PRL and IL-2 to activate proteinStat proteins in different T cell lines .
0.9033 1.0000 1.0000 We investigated the ability of PRL and proteinIL-2 to activate Stat proteins in different T cell lines .
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0.9575 1.0000 1.0000 The DNA binding specificities, the reactivities toward Stat-specific antisera , and the mol wt of IL-2 -and proteinPRL -induced DNA-binding proteins in Nb2 and C196 T cell lines were investigated.
0.9376 1.0000 1.0000 The DNA binding specificities, the reactivities toward Stat-specific antisera , and the mol wt of proteinIL-2 -and PRL -induced DNA-binding proteins in Nb2 and C196 T cell lines were investigated.
The DNA binding specificities, the reactivities toward Stat-specific antisera , and the mol wt of IL-2 -and proteinPRL -induced DNA-binding proteins in Nb2 and C196 T cell lines were investigated.
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3.9427 20.6540 10.6383 A comparison with the Stat proteins induced by interferon-gamma , PRL , and IL-6 in cell_lineT47D mammary tumor cells was made.
1.9449 20.1959 0.9999 A comparison with the proteinStat proteins induced by interferon-gamma , PRL , and IL-6 in T47D mammary tumor cells was made.
1.5381 10.4716 1.0000 A comparison with the Stat proteins induced by interferon-gamma , PRL , and proteinIL-6 in T47D mammary tumor cells was made.
0.9351 1.0000 1.0000 A comparison with the Stat proteins induced by interferon-gamma , proteinPRL , and IL-6 in T47D mammary tumor cells was made.
0.8509 1.0000 1.0000 A comparison with the Stat proteins induced by proteininterferon-gamma , PRL , and IL-6 in T47D mammary tumor cells was made.
Cls_Score Left_Reg_Score Right_Reg_Score Text
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3.5698 20.8722 10.5341 A transcription factor closely related to proteinmammary gland factor-Stat5 is rapidly activated upon interaction of IL-2 and PRL with their respective receptors.
0.8995 1.0000 1.0000 A transcription factor closely related to mammary gland factor-Stat5 is rapidly activated upon interaction of IL-2 and proteinPRL with their respective receptors.
0.8676 0.9999 1.0000 A transcription factor closely related to mammary gland factor-Stat5 is rapidly activated upon interaction of proteinIL-2 and PRL with their respective receptors.
1.3875 10.7829 0.9999 A proteintranscription factor closely related to mammary gland factor-Stat5 is rapidly activated upon interaction of IL-2 and PRL with their respective receptors.
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1.5706 10.4216 1.0000 Activation of a second protein related to proteinStat1 was also observed.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1515 20.4377 0.9992 Our results emphasize the role of PRL as a regulator of the immune response and indicate that the proteinStat factors mammary gland factor-Stat5 and Stat1 play a role in the regulation of gene expression during T cell development .
1.7636 10.0207 1.0000 Our results emphasize the role of proteinPRL as a regulator of the immune response and indicate that the Stat factors mammary gland factor-Stat5 and Stat1 play a role in the regulation of gene expression during T cell development .
1.4829 0.9672 10.5983 Our results emphasize the role of PRL as a regulator of the immune response and indicate that the Stat factors proteinmammary gland factor-Stat5 and Stat1 play a role in the regulation of gene expression during T cell development .
0.9716 1.0000 1.0000 Our results emphasize the role of PRL as a regulator of the immune response and indicate that the Stat factors mammary gland factor-Stat5 and proteinStat1 play a role in the regulation of gene expression during T cell development .
0.9578 1.0000 1.0000 Our results emphasize the role of PRL as a regulator of the immune response and indicate that the Stat factors mammary gland proteinfactor-Stat5 and Stat1 play a role in the regulation of gene expression during T cell development .
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3.4554 20.3796 10.6144 ETS1 transactivates the human GM-CSF promoter in cell_lineJurkat T cells stimulated with PMA and ionomycin .
3.2372 20.6165 10.4266 ETS1 transactivates the DNAhuman GM-CSF promoter in Jurkat T cells stimulated with PMA and ionomycin .
0.9563 1.0000 1.0000 proteinETS1 transactivates the human GM-CSF promoter in Jurkat T cells stimulated with PMA and ionomycin .
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2.2575 20.9258 10.2718 Activation of cell_typeT helper cells results in coordinate expression of a number of cytokines involved in differentiation , proliferation and activation of the haematopoietic system .
1.6266 10.6609 1.0000 Activation of T helper cells results in coordinate expression of a number of proteincytokines involved in differentiation , proliferation and activation of the haematopoietic system .
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1.6245 10.1559 1.0000 Granulocyte-macrophage colony-stimulating factor ( GM-CSF ) is one such proteincytokine whose increased expression results partly from increases in transcription .
1.5840 0.9988 10.2136 proteinGranulocyte-macrophage colony-stimulating factor ( GM-CSF ) is one such cytokine whose increased expression results partly from increases in transcription .
0.9738 1.0000 1.0000 Granulocyte-macrophage colony-stimulating factor ( proteinGM-CSF ) is one such cytokine whose increased expression results partly from increases in transcription .
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1.5914 10.9495 0.9964 Cis-acting elements with NF kappa B , AP-1 and ETS-like motifs have been identified in the promoter region of the proteinGM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
1.5462 10.8773 1.0000 Cis-acting elements with NF kappa B , AP-1 and ETS-like motifs have been identified in the promoter region of the DNAGM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
0.8716 0.9991 0.9999 DNACis-acting elements with NF kappa B , AP-1 and ETS-like motifs have been identified in the promoter region of the GM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
1.5505 10.9563 0.9999 Cis-acting elements with NF kappa B , AP-1 and ETS-like motifs have been identified in the DNApromoter region of the GM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
Cis-acting elements with NF kappa B , proteinAP-1 and ETS-like motifs have been identified in the promoter region of the GM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
Cis-acting elements with NF kappa B , AP-1 and DNAETS-like motifs have been identified in the promoter region of the GM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
Cis-acting elements with proteinNF kappa B , AP-1 and ETS-like motifs have been identified in the promoter region of the GM-CSF gene , which are important for transcriptional activity following PMA and ionomycin stimulation.
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2.1717 20.4526 0.9999 A number of the ETS family of transcription factors are expressed in cell_typeT cells , including ETS1 and ELF1 .
1.9851 20.7249 0.9999 A number of the proteinETS family of transcription factors are expressed in T cells , including ETS1 and ELF1 .
1.6094 10.3253 1.0000 A number of the ETS family of transcription factors are expressed in T cells , including proteinETS1 and ELF1 .
1.4286 10.5914 0.9999 A number of the ETS family of proteintranscription factors are expressed in T cells , including ETS1 and ELF1 .
0.8826 1.0000 1.0000 A number of the ETS family of transcription factors are expressed in T cells , including ETS1 and proteinELF1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9556 20.4645 10.9823 Here we describe the ability of these factors to interact with a site ( GM5 ), located within the CLE0 element , -47 to -40 upstream of the DNAGM-CSF transcription initiation site .
3.2292 10.7851 10.7600 Here we describe the ability of these factors to interact with a site ( GM5 ), located within the CLE0 element , DNA-47 to -40 upstream of the GM-CSF transcription initiation site .
2.1952 20.0053 0.9982 Here we describe the ability of these factors to interact with a site ( GM5 ), located within the CLE0 element , -47 to -40 upstream of the proteinGM-CSF transcription initiation site .
1.9744 20.0091 0.9999 Here we describe the ability of these factors to interact with a site ( GM5 ), located within the DNACLE0 element , -47 to -40 upstream of the GM-CSF transcription initiation site .
0.8714 1.0000 1.0000 Here we describe the ability of these factors to interact with a site ( DNAGM5 ), located within the CLE0 element , -47 to -40 upstream of the GM-CSF transcription initiation site .
1.9337 20.0458 0.9648 Here we describe the ability of these factors to interact with a site ( GM5 ), located within the DNACLE0 element , -47 to -40 upstream of the GM-CSF transcription initiation site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2299 20.4570 0.9999 Exogenous ETS1 , but not ELF1 , can transactivate GM-CSF , through the DNAGM5 site, in a PMA / ionomycin dependent manner .
1.7467 10.0467 1.0000 Exogenous proteinETS1 , but not ELF1 , can transactivate GM-CSF , through the GM5 site, in a PMA / ionomycin dependent manner .
1.5964 10.7570 1.0000 Exogenous ETS1 , but not proteinELF1 , can transactivate GM-CSF , through the GM5 site, in a PMA / ionomycin dependent manner .
0.8518 1.0000 1.0000 Exogenous ETS1 , but not ELF1 , can transactivate proteinGM-CSF , through the GM5 site, in a PMA / ionomycin dependent manner .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1694 20.0607 0.9999 Other unidentified ETS-like factors present in cell_lineJurkat cells are also capable of binding GM5 .
2.0480 20.6650 0.9999 Other unidentified proteinETS-like factors present in Jurkat cells are also capable of binding GM5 .
Other unidentified ETS-like factors present in Jurkat cells are also capable of binding DNAGM5 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7082 20.6166 10.7403 Mutation of the core DNAETS binding site from -GGAA- to -GGAT- prevents the binding of ETS-like factors with the exception of ETS1 .
2.0515 20.7681 1.0000 Mutation of the core ETS binding site from -GGAA- to -GGAT- prevents the binding of proteinETS-like factors with the exception of ETS1 .
1.9258 20.1241 1.0000 Mutation of the core ETS binding site from -GGAA- to -GGAT- prevents the binding of ETS-like factors with the exception of proteinETS1 .
Mutation of the core ETS binding site from DNA-GGAA- to -GGAT- prevents the binding of ETS-like factors with the exception of ETS1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7555 10.4215 1.0000 The GM-CSF promoter , modified in this way to be ETS1 specific , is fully responsive to PMA / ionomycin induction, in addition to proteinETS1 transactivation in the presence of PMA and ionomycin .
1.6411 10.7578 1.0000 The DNAGM-CSF promoter , modified in this way to be ETS1 specific , is fully responsive to PMA / ionomycin induction, in addition to ETS1 transactivation in the presence of PMA and ionomycin .
1.5699 10.9293 0.9867 The proteinGM-CSF promoter , modified in this way to be ETS1 specific , is fully responsive to PMA / ionomycin induction, in addition to ETS1 transactivation in the presence of PMA and ionomycin .
0.9039 1.0000 1.0000 The GM-CSF promoter , modified in this way to be proteinETS1 specific , is fully responsive to PMA / ionomycin induction, in addition to ETS1 transactivation in the presence of PMA and ionomycin .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7598 10.3973 1.0000 Together these data suggest that ETS1 may be involved in mediating the increased proteinGM-CSF production associated with T cell activation .
1.6575 10.6637 1.0000 Together these data suggest that proteinETS1 may be involved in mediating the increased GM-CSF production associated with T cell activation .
Together these data suggest that ETS1 may be involved in mediating the increased GM-CSF production associated with cell_typeT cell activation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9152 10.9988 10.8586 Quantitation of proteinbeta 1 triiodothyronine receptor mRNA in human tissues by competitive reverse transcription polymerase chain reaction .
1.6241 10.6766 0.9995 Quantitation of RNAbeta 1 triiodothyronine receptor mRNA in human tissues by competitive reverse transcription polymerase chain reaction .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5129 20.3709 10.8045 Thyroid hormones act by binding to proteinnuclear receptor proteins , the thyroid hormone receptors ( TR ) alpha and beta .
1.8315 10.9957 10.5907 Thyroid hormones act by binding to nuclear receptor proteins , the proteinthyroid hormone receptors ( TR ) alpha and beta .
0.9075 1.0000 1.0000 Thyroid hormones act by binding to nuclear receptor proteins , the thyroid hormone receptors ( proteinTR ) alpha and beta .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9446 1.0000 1.0000 Data from cell culture and animal studies indicate that proteinTR expression may be regulated to modulate target organ responsiveness to thyroid hormone .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0077 20.4928 10.5133 To investigate whether such adaptive changes in TR expression occur in humans, we determined the mRNA levels of the proteinhTR beta 1 in various thyroid states .
1.7456 10.3908 1.0000 To investigate whether such adaptive changes in proteinTR expression occur in humans, we determined the mRNA levels of the hTR beta 1 in various thyroid states .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2885 20.2464 10.8875 Total RNA was isolated from cell_typeperipheral blood mononuclear cells and hTR beta 1 mRNA levels determined by quantitative competitive reverse transcription PCR .
2.7697 20.6968 10.7563 Total RNA was isolated from peripheral blood mononuclear cells and proteinhTR beta 1 mRNA levels determined by quantitative competitive reverse transcription PCR .
2.4586 20.7683 0.9999 Total RNA was isolated from peripheral blood mononuclear cells and RNAhTR beta 1 mRNA levels determined by quantitative competitive reverse transcription PCR .
0.8528 0.9995 1.0000 Total RNARNA was isolated from peripheral blood mononuclear cells and hTR beta 1 mRNA levels determined by quantitative competitive reverse transcription PCR .
RNATotal RNA was isolated from peripheral blood mononuclear cells and hTR beta 1 mRNA levels determined by quantitative competitive reverse transcription PCR .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3778 20.4519 10.6062 For comparison, proteinhTR beta 1 mRNA levels were determined in lymphocytes and normal thyroid tissue of euthyroid patients .
2.3773 20.3171 0.9997 For comparison, RNAhTR beta 1 mRNA levels were determined in lymphocytes and normal thyroid tissue of euthyroid patients .
1.6722 10.1168 1.0000 For comparison, hTR beta 1 mRNA levels were determined in cell_typelymphocytes and normal thyroid tissue of euthyroid patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7077 10.4939 1.0000 Human TR beta 1 mRNA levels in cell_typelymphocytes were 1.8 +/- 0.4, 1.9 +/- 0.5, 1.1 +/- 0.4 10(-18) mol/microgram RNA in hypo -, eu -and hyper thyroid patients , respectively, corresponding to an estimated 0.5 -2 molecules per cell.
1.7064 0.9995 10.7002 proteinHuman TR beta 1 mRNA levels in lymphocytes were 1.8 +/- 0.4, 1.9 +/- 0.5, 1.1 +/- 0.4 10(-18) mol/microgram RNA in hypo -, eu -and hyper thyroid patients , respectively, corresponding to an estimated 0.5 -2 molecules per cell.
0.8183 0.9903 0.9982 RNAHuman TR beta 1 mRNA levels in lymphocytes were 1.8 +/- 0.4, 1.9 +/- 0.5, 1.1 +/- 0.4 10(-18) mol/microgram RNA in hypo -, eu -and hyper thyroid patients , respectively, corresponding to an estimated 0.5 -2 molecules per cell.
0.8588 0.9998 1.0000 Human TR beta 1 mRNA levels in lymphocytes were 1.8 +/- 0.4, 1.9 +/- 0.5, 1.1 +/- 0.4 10(-18) mol/microgram RNARNA in hypo -, eu -and hyper thyroid patients , respectively, corresponding to an estimated 0.5 -2 molecules per cell.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5815 20.6008 10.8226 Although the mean proteinhTR beta 1 mRNA levels were 40% lower in hyperthyroid than in euthyroid subjects, this difference did not reach statistical significance .
2.4310 20.7290 0.9998 Although the mean RNAhTR beta 1 mRNA levels were 40% lower in hyperthyroid than in euthyroid subjects, this difference did not reach statistical significance .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3587 20.9945 10.7661 Similar levels of proteinhTR beta 1 mRNA levels were detected in thyroid gland from euthyroid patients .
2.2863 20.9049 0.9999 Similar levels of RNAhTR beta 1 mRNA levels were detected in thyroid gland from euthyroid patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7193 20.8373 10.9811 In summary, we developed an assay for the quantitative determination of proteinhTR beta 1 mRNA levels in small human tissue samples , containing as little as 50 ng of total RNA.
2.4590 20.8313 0.9999 In summary, we developed an assay for the quantitative determination of RNAhTR beta 1 mRNA levels in small human tissue samples , containing as little as 50 ng of total RNA.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2523 20.9302 10.9724 Absolute hTR beta 1 mRNA levels are very low with an estimated one molecule of mRNA being present in a cell_typemononuclear blood cell or thyrocyte .
3.5243 10.8234 20.2076 Absolute RNAhTR beta 1 mRNA levels are very low with an estimated one molecule of mRNA being present in a mononuclear blood cell or thyrocyte .
1.7191 10.0082 0.9999 Absolute hTR beta 1 mRNA levels are very low with an estimated one molecule of mRNA being present in a mononuclear blood cell or cell_typethyrocyte .
1.6780 10.7857 1.0000 Absolute hTR beta 1 mRNA levels are very low with an estimated one molecule of RNAmRNA being present in a mononuclear blood cell or thyrocyte .
1.2644 0.9959 10.1076 Absolute proteinhTR beta 1 mRNA levels are very low with an estimated one molecule of mRNA being present in a mononuclear blood cell or thyrocyte .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8460 20.5841 10.6886 No up-regulation of proteinhTR beta 1 was seen in hypothyroid relative to euthyroid patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6607 20.6143 10.9392 However, there is a non-significant trend towards a down-regulation of proteinhTR beta 1 mRNA levels in hyperthyroid patients .
2.3983 20.4763 0.9999 However, there is a non-significant trend towards a down-regulation of RNAhTR beta 1 mRNA levels in hyperthyroid patients .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.9317 20.9620 20.5675 Multiple proteins interact with the DNAnuclear inhibitory protein repressor element in the human interleukin-3 promoter .
3.6220 30.9054 10.4047 Multiple proteins interact with the nuclear inhibitory protein repressor element in the DNAhuman interleukin-3 promoter .
Multiple proteinproteins interact with the nuclear inhibitory protein repressor element in the human interleukin-3 promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6701 20.8957 10.4465 T cell expression of interleukin 3 ( IL-3 ) is directed by positive and negative cis-acting DNA elements clustered within 300 base pairs of the DNAtranscriptional start site .
2.3257 20.8363 1.0000 T cell expression of proteininterleukin 3 ( IL-3 ) is directed by positive and negative cis-acting DNA elements clustered within 300 base pairs of the transcriptional start site .
0.9786 1.0000 1.0000 T cell expression of interleukin 3 ( proteinIL-3 ) is directed by positive and negative cis-acting DNA elements clustered within 300 base pairs of the transcriptional start site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6539 30.4434 10.8456 A strong repressor element , termed proteinnuclear inhibitory protein ( NIP ), was previously mapped to a segment of the IL-3 promoter between nucleotides -271 and -250 .
3.0543 10.2493 20.0980 A strong repressor element , termed nuclear inhibitory protein ( NIP ), was previously mapped to a segment of the IL-3 promoter between DNAnucleotides -271 and -250 .
1.9696 20.7445 0.9998 A strong repressor element , termed nuclear inhibitory protein ( NIP ), was previously mapped to a segment of the DNAIL-3 promoter between nucleotides -271 and -250 .
0.9692 1.0000 1.0000 A strong repressor element , termed nuclear inhibitory protein ( proteinNIP ), was previously mapped to a segment of the IL-3 promoter between nucleotides -271 and -250 .
1.9222 20.7431 0.9601 A strong repressor element , termed nuclear inhibitory protein ( NIP ), was previously mapped to a segment of the proteinIL-3 promoter between nucleotides -271 and -250 .
A strong proteinrepressor element , termed nuclear inhibitory protein ( NIP ), was previously mapped to a segment of the IL-3 promoter between nucleotides -271 and -250 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3840 20.1438 0.9999 Functional characterization of this element demonstrates that it can mediate repression when linked in cis to a DNAheterologous promoter .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4959 20.0975 1.0000 Using varying conditions, three distinct complexes were shown to interact specifically with the DNANIP region , although only one correlates with repressor activity .
Using varying conditions, three distinct complexes were shown to interact specifically with the proteinNIP region , although only one correlates with repressor activity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4200 20.2636 1.0000 Complex 1 results from binding of a ubiquitous polypeptide that recognizes the DNA3' portion of this sequence and is not required for repression .
0.9202 1.0000 1.0000 proteinComplex 1 results from binding of a ubiquitous polypeptide that recognizes the 3' portion of this sequence and is not required for repression .
1.4138 10.9255 0.9999 Complex 1 results from binding of a proteinubiquitous polypeptide that recognizes the 3' portion of this sequence and is not required for repression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6304 20.5629 10.3535 Complex 2 corresponds to binding of transcription factor ( proteinupstream stimulatory factor ) to an E-box motif in the 5' portion of the NIP region .
2.1181 20.4177 0.9999 Complex 2 corresponds to binding of transcription factor ( upstream stimulatory factor ) to an E-box motif in the DNA5' portion of the NIP region .
2.1030 20.1423 0.9998 Complex 2 corresponds to binding of transcription factor ( upstream stimulatory factor ) to an E-box motif in the 5' portion of the DNANIP region .
2.0533 20.5511 0.9999 Complex 2 corresponds to binding of transcription factor ( upstream stimulatory factor ) to an DNAE-box motif in the 5' portion of the NIP region .
2.0315 20.1871 0.9999 Complex 2 corresponds to binding of proteintranscription factor ( upstream stimulatory factor ) to an E-box motif in the 5' portion of the NIP region .
0.8011 1.0000 1.0000 proteinComplex 2 corresponds to binding of transcription factor ( upstream stimulatory factor ) to an E-box motif in the 5' portion of the NIP region .
Complex 2 corresponds to binding of transcription factor ( upstream stimulatory factor ) to an E-box motif in the 5' portion of the proteinNIP region .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5619 20.2756 10.4278 DNA binding specificity of complex 3 overlaps with that of proteinupstream stimulatory factor but is clearly distinct.
2.1825 20.2988 1.0000 DNA binding specificity of proteincomplex 3 overlaps with that of upstream stimulatory factor but is clearly distinct.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.1528 20.5854 10.7098 To determine which of the latter two complexes represents NIP activity , we incorporated small alterations into the NIP site of an DNAIL-3 promoter -linked reporter construct and examined their effects on NIP -mediated repression .
2.1826 20.3967 0.9999 To determine which of the latter two complexes represents NIP activity , we incorporated small alterations into the DNANIP site of an IL-3 promoter -linked reporter construct and examined their effects on NIP -mediated repression .
2.0144 20.4688 0.9814 To determine which of the latter two complexes represents NIP activity , we incorporated small alterations into the NIP site of an DNAIL-3 promoter -linked reporter construct and examined their effects on NIP -mediated repression .
1.6028 10.2047 1.0000 To determine which of the latter two complexes represents proteinNIP activity , we incorporated small alterations into the NIP site of an IL-3 promoter -linked reporter construct and examined their effects on NIP -mediated repression .
0.8614 1.0000 1.0000 To determine which of the latter two complexes represents NIP activity , we incorporated small alterations into the NIP site of an IL-3 promoter -linked reporter construct and examined their effects on proteinNIP -mediated repression .
1.9046 20.6096 0.9791 To determine which of the latter two complexes represents NIP activity , we incorporated small alterations into the NIP site of an proteinIL-3 promoter -linked reporter construct and examined their effects on NIP -mediated repression .
To determine which of the latter two complexes represents NIP activity , we incorporated small alterations into the proteinNIP site of an IL-3 promoter -linked reporter construct and examined their effects on NIP -mediated repression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2998 20.3573 1.0000 Functional specificity for repression matches the DNA binding specificity of proteincomplex 3 ; both repressor activity and complex 3 binding require the consensus sequence CTCACNTNC .
2.2907 20.2520 1.0000 Functional specificity for repression matches the DNA binding specificity of complex 3 ; both repressor activity and proteincomplex 3 binding require the consensus sequence CTCACNTNC .
2.1928 20.8914 0.9990 Functional specificity for repression matches the DNA binding specificity of complex 3 ; both repressor activity and complex 3 binding require the DNAconsensus sequence CTCACNTNC .
0.7903 0.9999 0.9999 Functional specificity for repression matches the DNA binding specificity of complex 3 ; both repressor activity and complex 3 binding require the consensus sequence DNACTCACNTNC .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.7626 30.2915 20.7020 The hematopoietic transcription factor PU.1 is downregulated in cell_linehuman multiple myeloma cell lines .
1.8730 10.9436 10.0474 The proteinhematopoietic transcription factor PU.1 is downregulated in human multiple myeloma cell lines .
0.9436 0.9998 1.0000 The hematopoietic transcription factor proteinPU.1 is downregulated in human multiple myeloma cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1776 20.0414 10.8303 PU.1 is a proteinhematopoietic transcription factor belonging to the Ets-family .
1.2394 10.3424 1.0000 PU.1 is a hematopoietic transcription factor belonging to the proteinEts-family .
0.9661 1.0000 1.0000 proteinPU.1 is a hematopoietic transcription factor belonging to the Ets-family .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5012 10.8838 1.0000 It is identical to the DNASpi-1 oncogene , which is implicated in spleen focus-forming virus-induced murine erythroleukemias .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5984 10.9074 1.0000 PU.1 seems to be required for early development of multiple hematopoietic lineages , but its expression in cell_typemature cells is preferentially observed in cells of the B-cell-and monocyte/macrophage- differentiation lineage .
0.9787 1.0000 1.0000 proteinPU.1 seems to be required for early development of multiple hematopoietic lineages , but its expression in mature cells is preferentially observed in cells of the B-cell-and monocyte/macrophage- differentiation lineage .
2.4114 20.1232 1.0000 PU.1 seems to be required for early development of multiple cell_typehematopoietic lineages , but its expression in mature cells is preferentially observed in cells of the B-cell-and monocyte/macrophage- differentiation lineage .
PU.1 seems to be required for early development of cell_typemultiple hematopoietic lineages , but its expression in mature cells is preferentially observed in cells of the B-cell-and monocyte/macrophage- differentiation lineage .
PU.1 seems to be required for early development of multiple hematopoietic lineages , but its expression in mature cells is preferentially observed in cells of the cell_typeB-cell-and monocyte/macrophage- differentiation lineage .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6427 20.8553 10.9522 It binds the so-called Pu box , an important DNAtissue-specific regulatory DNA element present in a number of genes expressed in these cell lineages .
2.1249 20.2809 1.0000 It binds the so-called DNAPu box , an important tissue-specific regulatory DNA element present in a number of genes expressed in these cell lineages .
1.7646 10.6316 10.2259 It binds the so-called Pu box , an important tissue-specific regulatory DNA element present in a number of genes expressed in these cell_typecell lineages .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3322 20.4895 1.0000 We have analyzed the expression and activity of PU.1 during human B-cell development using a panel of cell_lineB-cell lines representing different stages of maturation, from early precursors to differentiated plasma cells .
1.7059 10.2289 1.0000 We have analyzed the expression and activity of proteinPU.1 during human B-cell development using a panel of B-cell lines representing different stages of maturation, from early precursors to differentiated plasma cells .
3.0182 10.6129 10.7660 We have analyzed the expression and activity of PU.1 during human B-cell development using a panel of B-cell lines representing different stages of maturation, from early precursors to cell_typedifferentiated plasma cells .
1.4848 10.6696 0.9994 We have analyzed the expression and activity of PU.1 during human B-cell development using a panel of B-cell lines representing different stages of maturation, from cell_typeearly precursors to differentiated plasma cells .
We have analyzed the expression and activity of PU.1 during human B-cell development using a panel of B-cell lines representing different stages of maturation, from early precursors to cell_linedifferentiated plasma cells .
We have analyzed the expression and activity of PU.1 during human B-cell development using a panel of B-cell lines representing different stages of maturation, from cell_lineearly precursors to differentiated plasma cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7767 10.4157 1.0000 PU.1 mRNA expression and proteinPU.1 DNA binding activity , as measured by Northern blot analysis and electrophoretic mobility shift assay , respectively, were evident in cell lines representing pro-B , pre-B , and mature B cells .
1.5882 10.8070 1.0000 PU.1 mRNA expression and PU.1 DNA binding activity , as measured by Northern blot analysis and electrophoretic mobility shift assay , respectively, were evident in cell_linecell lines representing pro-B , pre-B , and mature B cells .
0.9449 0.9995 1.0000 RNAPU.1 mRNA expression and PU.1 DNA binding activity , as measured by Northern blot analysis and electrophoretic mobility shift assay , respectively, were evident in cell lines representing pro-B , pre-B , and mature B cells .
0.8735 1.0000 0.9929 proteinPU.1 mRNA expression and PU.1 DNA binding activity , as measured by Northern blot analysis and electrophoretic mobility shift assay , respectively, were evident in cell lines representing pro-B , pre-B , and mature B cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3209 20.3896 0.9998 We could also show Pu box -dependent transactivation of a reporter gene in transient transfections in these cell_linecell lines .
2.3116 20.5867 0.9999 We could also show DNAPu box -dependent transactivation of a reporter gene in transient transfections in these cell lines .
2.2498 20.5143 1.0000 We could also show Pu box -dependent transactivation of a DNAreporter gene in transient transfections in these cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.3025 30.4197 20.3585 In contrast, in a number of multiple myeloma cell lines , representing cell_typedifferentiated, plasma cell-like B cells , PU.1 DNA binding activity , mRNA expression , and Pu box -dependent transactivation were absent or detectable at a very low level.
4.5542 20.7285 10.4974 In contrast, in a number of cell_linemultiple myeloma cell lines , representing differentiated, plasma cell-like B cells , PU.1 DNA binding activity , mRNA expression , and Pu box -dependent transactivation were absent or detectable at a very low level.
1.9719 20.2615 0.9999 In contrast, in a number of multiple myeloma cell lines , representing differentiated, plasma cell-like B cells , PU.1 DNA binding activity , mRNA expression , and DNAPu box -dependent transactivation were absent or detectable at a very low level.
0.9580 1.0000 1.0000 In contrast, in a number of multiple myeloma cell lines , representing differentiated, plasma cell-like B cells , proteinPU.1 DNA binding activity , mRNA expression , and Pu box -dependent transactivation were absent or detectable at a very low level.
1.1704 0.9999 10.8633 In contrast, in a number of multiple myeloma cell lines , representing differentiated, cell_typeplasma cell-like B cells , PU.1 DNA binding activity , mRNA expression , and Pu box -dependent transactivation were absent or detectable at a very low level.
0.6279 0.9965 0.9996 In contrast, in a number of multiple myeloma cell lines , representing differentiated, plasma cell-like cell_typeB cells , PU.1 DNA binding activity , mRNA expression , and Pu box -dependent transactivation were absent or detectable at a very low level.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2644 10.8325 10.6183 In cell_linelymphoblastoid cell lines , which exemplify an intermediate stage of B-cell differentiation , a reduced expression and activity were observed.
Cls_Score Left_Reg_Score Right_Reg_Score Text
7.2375 30.8282 20.5032 The findings in the cell_linehuman multiple myeloma cell lines represent the first examples of B cells with downregulated PU.1 expression and apparently contradict observations in the murine system in which PU.1 is expressed and active in plasmacytoma cell lines .
3.5516 20.5279 10.7551 The findings in the human multiple myeloma cell lines represent the first examples of B cells with downregulated PU.1 expression and apparently contradict observations in the murine system in which PU.1 is expressed and active in cell_lineplasmacytoma cell lines .
2.1852 20.2221 0.9999 The findings in the human multiple myeloma cell lines represent the first examples of cell_typeB cells with downregulated PU.1 expression and apparently contradict observations in the murine system in which PU.1 is expressed and active in plasmacytoma cell lines .
1.6364 10.4367 1.0000 The findings in the human multiple myeloma cell lines represent the first examples of B cells with downregulated proteinPU.1 expression and apparently contradict observations in the murine system in which PU.1 is expressed and active in plasmacytoma cell lines .
0.8663 1.0000 1.0000 The findings in the human multiple myeloma cell lines represent the first examples of B cells with downregulated PU.1 expression and apparently contradict observations in the murine system in which proteinPU.1 is expressed and active in plasmacytoma cell lines .
The findings in the human cell_linemultiple myeloma cell lines represent the first examples of B cells with downregulated PU.1 expression and apparently contradict observations in the murine system in which PU.1 is expressed and active in plasmacytoma cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.6367 20.8431 20.1368 At present, it is unclear whether the lack of PU.1 expression and activity in cell_linehuman multiple myeloma cell lines represents a malignancy-associated defect in these cells or exemplifies a normal developmental regulation in terminally differentiated B cells .
3.7622 20.5554 10.9244 At present, it is unclear whether the lack of PU.1 expression and activity in human multiple myeloma cell lines represents a malignancy-associated defect in these cells or exemplifies a normal developmental regulation in cell_typeterminally differentiated B cells .
1.5204 10.3498 1.0000 At present, it is unclear whether the lack of proteinPU.1 expression and activity in human multiple myeloma cell lines represents a malignancy-associated defect in these cells or exemplifies a normal developmental regulation in terminally differentiated B cells .
1.4938 0.9999 10.0650 At present, it is unclear whether the lack of PU.1 expression and activity in human multiple myeloma cell lines represents a malignancy-associated defect in these cells or exemplifies a normal developmental regulation in terminally differentiated cell_typeB cells .
At present, it is unclear whether the lack of PU.1 expression and activity in human cell_linemultiple myeloma cell lines represents a malignancy-associated defect in these cells or exemplifies a normal developmental regulation in terminally differentiated B cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0493 20.8367 10.9951 Regulation of granulocyte-macrophage colony-stimulating factor and E-selectin expression in endothelial cells by cyclosporin A and the proteinT-cell transcription factor NFAT .
4.0247 20.5599 10.9046 Regulation of proteingranulocyte-macrophage colony-stimulating factor and E-selectin expression in endothelial cells by cyclosporin A and the T-cell transcription factor NFAT .
1.3879 10.5929 0.9999 Regulation of granulocyte-macrophage colony-stimulating factor and E-selectin expression in cell_typeendothelial cells by cyclosporin A and the T-cell transcription factor NFAT .
0.9528 0.9999 0.9999 Regulation of granulocyte-macrophage colony-stimulating factor and E-selectin expression in endothelial cells by cyclosporin A and the T-cell transcription factor proteinNFAT .
0.9106 1.0000 1.0000 Regulation of granulocyte-macrophage colony-stimulating factor and proteinE-selectin expression in endothelial cells by cyclosporin A and the T-cell transcription factor NFAT .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9280 30.1450 10.3180 Nuclear factor of activated T cells ( NFAT ) was originally described as a proteinT-cell-specific transcription factor athat supported the activation of cytokine gene expression and mediated the immunoregulatory effects of cyclosporin A ( CsA ).
2.5989 0.9988 20.2860 proteinNuclear factor of activated T cells ( NFAT ) was originally described as a T-cell-specific transcription factor athat supported the activation of cytokine gene expression and mediated the immunoregulatory effects of cyclosporin A ( CsA ).
0.9842 1.0000 1.0000 Nuclear factor of activated T cells ( proteinNFAT ) was originally described as a T-cell-specific transcription factor athat supported the activation of cytokine gene expression and mediated the immunoregulatory effects of cyclosporin A ( CsA ).
0.7943 0.9998 1.0000 Nuclear factor of activated T cells ( NFAT ) was originally described as a T-cell-specific transcription factor athat supported the activation of cytokine gene expression and mediated the proteinimmunoregulatory effects of cyclosporin A ( CsA ).
1.2550 10.9427 0.9998 Nuclear factor of activated T cells ( NFAT ) was originally described as a T-cell-specific transcription factor athat supported the activation of DNAcytokine gene expression and mediated the immunoregulatory effects of cyclosporin A ( CsA ).
Nuclear factor of activated T cells ( NFAT ) was originally described as a T-cell-specific transcription factor athat supported the activation of proteincytokine gene expression and mediated the immunoregulatory effects of cyclosporin A ( CsA ).
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2.2132 20.5410 0.9998 As we observed that activated endothelial cells also expressed NFAT , we tested the antiinflammatory properties of CsA in cell_typeendothelial cells .
1.6813 10.4544 1.0000 As we observed that activated endothelial cells also expressed proteinNFAT , we tested the antiinflammatory properties of CsA in endothelial cells .
2.2620 20.1633 0.9999 As we observed that activated cell_typeendothelial cells also expressed NFAT , we tested the antiinflammatory properties of CsA in endothelial cells .
As we observed that cell_typeactivated endothelial cells also expressed NFAT , we tested the antiinflammatory properties of CsA in endothelial cells .
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5.7470 30.2281 20.9086 Significantly, CsA completely suppressed the induction of NFAT in endothelial cells and inhibited the activity of DNAgranulocyte-macrophage colony-stimulating factor ( GM-CSF ) gene regulatory elements that use NFAT by 60%.
3.6928 30.9553 10.5514 Significantly, CsA completely suppressed the induction of NFAT in endothelial cells and inhibited the activity of proteingranulocyte-macrophage colony-stimulating factor ( GM-CSF ) gene regulatory elements that use NFAT by 60%.
1.3192 10.2259 1.0000 Significantly, CsA completely suppressed the induction of proteinNFAT in endothelial cells and inhibited the activity of granulocyte-macrophage colony-stimulating factor ( GM-CSF ) gene regulatory elements that use NFAT by 60%.
1.1846 10.2367 0.9997 Significantly, CsA completely suppressed the induction of NFAT in cell_typeendothelial cells and inhibited the activity of granulocyte-macrophage colony-stimulating factor ( GM-CSF ) gene regulatory elements that use NFAT by 60%.
0.9505 1.0000 0.9976 Significantly, CsA completely suppressed the induction of NFAT in endothelial cells and inhibited the activity of granulocyte-macrophage colony-stimulating factor ( proteinGM-CSF ) gene regulatory elements that use NFAT by 60%.
0.6833 0.9997 1.0000 Significantly, CsA completely suppressed the induction of NFAT in endothelial cells and inhibited the activity of granulocyte-macrophage colony-stimulating factor ( GM-CSF ) gene regulatory elements that use proteinNFAT by 60%.
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2.4945 20.1560 1.0000 CsA similarly mediated a reduction of up to 65% in RNAGM-CSF mRNA and protein expression in activated endothelial cells .
2.0461 20.3495 0.9938 CsA similarly mediated a reduction of up to 65% in proteinGM-CSF mRNA and protein expression in activated endothelial cells .
0.7892 0.9993 0.9998 CsA similarly mediated a reduction of up to 65% in GM-CSF mRNA and protein expression in activated cell_typeendothelial cells .
CsA similarly mediated a reduction of up to 65% in GM-CSF mRNA and protein expression in cell_typeactivated endothelial cells .
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4.4532 20.9296 10.7071 CsA also suppressed E-selectin , but not proteinvascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the E-selectin promoter is activated by NF-kappa B rather than NFAT .
2.0931 20.2995 1.0000 CsA also suppressed E-selectin , but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the E-selectin promoter is activated by proteinNF-kappa B rather than NFAT .
2.0216 20.3117 0.9924 CsA also suppressed E-selectin , but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the proteinE-selectin promoter is activated by NF-kappa B rather than NFAT .
1.9960 20.3299 1.0000 CsA also suppressed E-selectin , but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the DNAE-selectin promoter is activated by NF-kappa B rather than NFAT .
1.4791 10.4305 1.0000 CsA also suppressed E-selectin , but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the E-selectin promoter is activated by NF-kappa B rather than proteinNFAT .
0.9619 1.0000 1.0000 CsA also suppressed E-selectin , but not vascular cell adhesion molecule-1 ( proteinVCAM-1 ) expression in endothelial cells, even though the E-selectin promoter is activated by NF-kappa B rather than NFAT .
0.8737 0.9999 1.0000 CsA also suppressed proteinE-selectin , but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the E-selectin promoter is activated by NF-kappa B rather than NFAT .
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4.3710 20.6890 10.6221 Hence, induction of cell surface expression of this proteinleukocyte adhesion molecule by tumor necrosis factor (TNF)-alpha was reduced by 40% in the presence of CsA , and this was reflected by a 29% decrease in neutrophil adhesion .
4.2192 20.9148 10.7554 Hence, induction of cell surface expression of this leukocyte adhesion molecule by proteintumor necrosis factor (TNF)-alpha was reduced by 40% in the presence of CsA , and this was reflected by a 29% decrease in neutrophil adhesion .
0.8012 0.9998 0.9999 Hence, induction of cell surface expression of this leukocyte adhesion molecule by tumor necrosis factor (TNF)-alpha was reduced by 40% in the presence of CsA , and this was reflected by a 29% decrease in cell_typeneutrophil adhesion .
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3.6103 20.2154 10.8259 The effects of CsA on endothelial cells were also detected at the chromatin structure level , as DNADNasel hypersensitive sites within both the GM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
1.4773 10.9940 0.9999 The effects of CsA on endothelial cells were also detected at the chromatin structure level , as DNasel hypersensitive sites within both the GM-CSF enhancer and the DNAE-selectin promoter were suppressed by CsA .
1.4389 10.8612 0.9999 The effects of CsA on cell_typeendothelial cells were also detected at the chromatin structure level , as DNasel hypersensitive sites within both the GM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
1.3946 10.8404 0.9912 The effects of CsA on endothelial cells were also detected at the chromatin structure level , as DNasel hypersensitive sites within both the proteinGM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
1.4502 10.7521 0.9999 The effects of CsA on endothelial cells were also detected at the DNAchromatin structure level , as DNasel hypersensitive sites within both the GM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
1.4404 10.9660 1.0000 The effects of CsA on endothelial cells were also detected at the chromatin structure level , as DNasel hypersensitive sites within both the DNAGM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
The effects of CsA on endothelial cells were also detected at the chromatin structure level , as DNasel hypersensitive sites within both the GM-CSF enhancer and the proteinE-selectin promoter were suppressed by CsA .
The effects of CsA on endothelial cells were also detected at the DNAchromatin structure level , as DNasel hypersensitive sites within both the GM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
The effects of CsA on endothelial cells were also detected at the chromatin structure level , as proteinDNasel hypersensitive sites within both the GM-CSF enhancer and the E-selectin promoter were suppressed by CsA .
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1.6437 10.7880 1.0000 This represents the first report of proteinNFAT in endothelial cells and suggests mechanisms by which CsA could function as an antiinflammatory agent .
1.6288 10.4434 0.9999 This represents the first report of NFAT in cell_typeendothelial cells and suggests mechanisms by which CsA could function as an antiinflammatory agent .
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1.5667 10.0853 1.0000 Costimulation requirement for proteinAP-1 and NF-kappa B transcription factor activation in T cells .
1.3977 10.8478 0.9993 Costimulation requirement for AP-1 and NF-kappa B transcription factor activation in cell_typeT cells .
1.3805 10.4122 0.9995 Costimulation requirement for AP-1 and proteinNF-kappa B transcription factor activation in T cells .
0.8318 0.9870 0.9999 Costimulation requirement for AP-1 and NF-kappa B proteintranscription factor activation in T cells .
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2.1251 20.1953 1.0000 The transcriptional activity of the DNAIL-2 promoter requires T-cell costimulation delivered by the TCR and the auxiliary receptor CD28 .
1.9955 20.0791 0.9909 The transcriptional activity of the proteinIL-2 promoter requires T-cell costimulation delivered by the TCR and the auxiliary receptor CD28 .
0.8784 1.0000 1.0000 The transcriptional activity of the IL-2 promoter requires T-cell costimulation delivered by the proteinTCR and the auxiliary receptor CD28 .
1.3539 10.5176 0.9994 The transcriptional activity of the IL-2 promoter requires T-cell costimulation delivered by the TCR and the proteinauxiliary receptor CD28 .
0.9717 0.9999 1.0000 The transcriptional activity of the IL-2 promoter requires T-cell costimulation delivered by the TCR and the auxiliary receptor proteinCD28 .
The transcriptional activity of the IL-2 promoter requires T-cell costimulation delivered by the TCR and the proteinauxiliary receptor CD28 .
The transcriptional activity of the IL-2 promoter requires cell_typeT-cell costimulation delivered by the TCR and the auxiliary receptor CD28 .
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2.6609 20.8542 10.8056 Several transcription factors participate in IL-2 promoter activation , among which are proteinAP-1 -like factors and NF-kappa B .
1.8674 20.3726 0.9952 Several transcription factors participate in IL-2 promoter activation , among which are proteinAP-1 -like factors and NF-kappa B .
1.8553 20.3371 0.9866 Several transcription factors participate in proteinIL-2 promoter activation , among which are AP-1 -like factors and NF-kappa B .
1.4651 10.9635 0.9998 Several transcription factors participate in IL-2 promoter activation , among which are AP-1 -like factors and proteinNF-kappa B .
1.3985 10.7834 0.9999 Several proteintranscription factors participate in IL-2 promoter activation , among which are AP-1 -like factors and NF-kappa B .
2.0227 20.3440 0.9999 Several transcription factors participate in DNAIL-2 promoter activation , among which are AP-1 -like factors and NF-kappa B .
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2.4208 10.3687 10.3042 Protein phosphorylation has an important role in the regulation of these two factors: (1) it induces the transactivating capacity of the AP-1 protein c-Jun ; and (2) it is involved in the release of the cytoplasmic inhibitor , proteinI kappa B , from NF-kappa B , allowing translocation of the latter into the nucleus .
2.3753 20.0637 1.0000 Protein phosphorylation has an important role in the regulation of these two factors: (1) it induces the transactivating capacity of the AP-1 protein c-Jun ; and (2) it is involved in the release of the cytoplasmic inhibitor , I kappa B , from proteinNF-kappa B , allowing translocation of the latter into the nucleus .
2.1408 20.5297 0.9977 Protein phosphorylation has an important role in the regulation of these two factors: (1) it induces the transactivating capacity of the proteinAP-1 protein c-Jun ; and (2) it is involved in the release of the cytoplasmic inhibitor , I kappa B , from NF-kappa B , allowing translocation of the latter into the nucleus .
1.5304 10.7542 1.0000 Protein phosphorylation has an important role in the regulation of these two factors: (1) it induces the transactivating capacity of the AP-1 protein c-Jun ; and (2) it is involved in the release of the proteincytoplasmic inhibitor , I kappa B , from NF-kappa B , allowing translocation of the latter into the nucleus .
0.9916 1.0000 1.0000 Protein phosphorylation has an important role in the regulation of these two factors: (1) it induces the transactivating capacity of the AP-1 protein proteinc-Jun ; and (2) it is involved in the release of the cytoplasmic inhibitor , I kappa B , from NF-kappa B , allowing translocation of the latter into the nucleus .
2.0502 20.6590 0.9899 Protein phosphorylation has an important role in the regulation of these two factors: (1) it induces the transactivating capacity of the proteinAP-1 protein c-Jun ; and (2) it is involved in the release of the cytoplasmic inhibitor , I kappa B , from NF-kappa B , allowing translocation of the latter into the nucleus .
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4.5093 20.2621 10.6890 Furthermore, in cell_typeactivated T cells , the kinetics of the two phosphorylation events are essentially similar.
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1.7570 10.0807 1.0000 According to our results, however, the proteinkinases responsible for the two processes are distinct entities.
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3.6819 20.8548 10.3915 Whereas TPCK inhibits phosphorylation of I kappa B and, consequently, activation of NF-kappa B , it markedly enhances the activity of JNK , the proteinMAP kinase-related kinase that phosphorylates the transactivation domain of c-Jun .
3.5194 20.9114 10.6684 Whereas TPCK inhibits phosphorylation of proteinI kappa B and, consequently, activation of NF-kappa B , it markedly enhances the activity of JNK , the MAP kinase-related kinase that phosphorylates the transactivation domain of c-Jun .
2.1525 20.3587 1.0000 Whereas TPCK inhibits phosphorylation of I kappa B and, consequently, activation of proteinNF-kappa B , it markedly enhances the activity of JNK , the MAP kinase-related kinase that phosphorylates the transactivation domain of c-Jun .
2.0440 20.7681 0.9999 Whereas TPCK inhibits phosphorylation of I kappa B and, consequently, activation of NF-kappa B , it markedly enhances the activity of JNK , the MAP kinase-related kinase that phosphorylates the proteintransactivation domain of c-Jun .
1.5428 10.0605 1.0000 Whereas TPCK inhibits phosphorylation of I kappa B and, consequently, activation of NF-kappa B , it markedly enhances the activity of JNK , the MAP kinase-related kinase that phosphorylates the transactivation domain of proteinc-Jun .
1.5028 10.6324 1.0000 Whereas TPCK inhibits phosphorylation of I kappa B and, consequently, activation of NF-kappa B , it markedly enhances the activity of proteinJNK , the MAP kinase-related kinase that phosphorylates the transactivation domain of c-Jun .
Whereas proteinTPCK inhibits phosphorylation of I kappa B and, consequently, activation of NF-kappa B , it markedly enhances the activity of JNK , the MAP kinase-related kinase that phosphorylates the transactivation domain of c-Jun .
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2.3501 20.1340 1.0000 Costimulation results in the activation of a signaling pathway that leads to the simultaneous induction of the two proteintranscription factors , AP-1 and NF-kappa B .
0.9726 1.0000 1.0000 Costimulation results in the activation of a signaling pathway that leads to the simultaneous induction of the two transcription factors , proteinAP-1 and NF-kappa B .
0.8415 0.9996 1.0000 Costimulation results in the activation of a signaling pathway that leads to the simultaneous induction of the two transcription factors , AP-1 and proteinNF-kappa B .
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3.7386 20.7821 10.9594 Integration of the signals generated by TCR and CD28 engagement occurs along this pathway, which then bifurcates to induce proteinI kappa B phosphorylation and NF-kappa B activation on the one hand, and JNK activation and c-Jun phosphorylation on the other.
2.2635 20.2105 1.0000 Integration of the signals generated by TCR and CD28 engagement occurs along this pathway, which then bifurcates to induce I kappa B phosphorylation and proteinNF-kappa B activation on the one hand, and JNK activation and c-Jun phosphorylation on the other.
1.6259 10.3494 1.0000 Integration of the signals generated by proteinTCR and CD28 engagement occurs along this pathway, which then bifurcates to induce I kappa B phosphorylation and NF-kappa B activation on the one hand, and JNK activation and c-Jun phosphorylation on the other.
1.6208 10.6468 1.0000 Integration of the signals generated by TCR and CD28 engagement occurs along this pathway, which then bifurcates to induce I kappa B phosphorylation and NF-kappa B activation on the one hand, and JNK activation and proteinc-Jun phosphorylation on the other.
0.8938 1.0000 1.0000 Integration of the signals generated by TCR and proteinCD28 engagement occurs along this pathway, which then bifurcates to induce I kappa B phosphorylation and NF-kappa B activation on the one hand, and JNK activation and c-Jun phosphorylation on the other.
0.8803 1.0000 1.0000 Integration of the signals generated by TCR and CD28 engagement occurs along this pathway, which then bifurcates to induce I kappa B phosphorylation and NF-kappa B activation on the one hand, and proteinJNK activation and c-Jun phosphorylation on the other.
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1.7322 10.1693 1.0000 We are currently engaged in defining where the two signals integrate along the proteinAP-1 / NF-kappa B pathway .
0.8929 0.9997 0.9997 We are currently engaged in defining where the two signals integrate along the AP-1 / proteinNF-kappa B pathway .
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2.0356 10.8238 10.0119 Regulation of human immunodeficiency virus type 1 and cytokine gene expression in cell_typemyeloid cells by NF-kappa B /Rel transcription factors .
1.3703 10.7841 0.9344 Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by proteinNF-kappa B /Rel transcription factors .
4.1354 20.5371 10.9843 Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by proteinNF-kappa B /Rel transcription factors .
1.3336 10.9700 0.9998 Regulation of human immunodeficiency virus type 1 and DNAcytokine gene expression in myeloid cells by NF-kappa B /Rel transcription factors .
Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by NF-kappa B /Rel proteintranscription factors .
Regulation of human immunodeficiency virus type 1 and cytokine gene expression in myeloid cells by proteinNF-kappa B /Rel transcription factors .
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3.8975 20.8660 10.5015 CD4+ macrophages in tissues such as lung , skin , and lymph nodes , promyelocytic cells in bone marrow , and cell_typeperipheral blood monocytes serve as important targets and reservoirs for human immunodeficiency virus type 1 ( HIV-1 ) replication .
2.3853 20.1178 0.9999 CD4+ macrophages in tissues such as lung , skin , and lymph nodes , cell_typepromyelocytic cells in bone marrow , and peripheral blood monocytes serve as important targets and reservoirs for human immunodeficiency virus type 1 ( HIV-1 ) replication .
0.9226 0.9994 1.0000 cell_typeCD4+ macrophages in tissues such as lung , skin , and lymph nodes , promyelocytic cells in bone marrow , and peripheral blood monocytes serve as important targets and reservoirs for human immunodeficiency virus type 1 ( HIV-1 ) replication .
cell_lineCD4+ macrophages in tissues such as lung , skin , and lymph nodes , promyelocytic cells in bone marrow , and peripheral blood monocytes serve as important targets and reservoirs for human immunodeficiency virus type 1 ( HIV-1 ) replication .
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1.7560 0.9986 10.5667 cell_typeHIV-1 -infected myeloid cells are often diminished in their ability to participate in chemotaxis , phagocytosis , and intracellular killing .
HIV-1 -infected cell_typemyeloid cells are often diminished in their ability to participate in chemotaxis , phagocytosis , and intracellular killing .
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2.4607 20.1822 1.0000 HIV-1 infection of myeloid cells can lead to the expression of proteinsurface receptors associated with cellular activation and/or differentiation that increase the responsiveness of these cells to cytokines secreted by neighboring cells as well as to bacteria or other pathogens.
2.4193 20.2436 1.0000 HIV-1 infection of cell_typemyeloid cells can lead to the expression of surface receptors associated with cellular activation and/or differentiation that increase the responsiveness of these cells to cytokines secreted by neighboring cells as well as to bacteria or other pathogens.
1.8070 10.5350 1.0000 HIV-1 infection of myeloid cells can lead to the expression of surface receptors associated with cellular activation and/or differentiation that increase the responsiveness of these cells to proteincytokines secreted by neighboring cells as well as to bacteria or other pathogens.
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3.7713 20.9816 10.9586 Enhancement of HIV-1 replication is related in part to increased DNA-binding activity of proteincellular transcription factors such as NF-kappa B .
2.1420 20.2476 0.9999 Enhancement of HIV-1 replication is related in part to increased DNA-binding activity of cellular transcription factors such as proteinNF-kappa B .
0.6471 0.9999 0.9999 Enhancement of HIV-1 replication is related in part to increased DNA-binding activity of cellular proteintranscription factors such as NF-kappa B .
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3.5881 20.5692 10.7895 NF-kappa B binds to the HIV-1 enhancer region of the DNAlong terminal repeat and contributes to the inducibility of HIV-1 gene expression in response to multiple activating agents.
0.9237 1.0000 1.0000 proteinNF-kappa B binds to the HIV-1 enhancer region of the long terminal repeat and contributes to the inducibility of HIV-1 gene expression in response to multiple activating agents.
2.9922 20.6168 10.5126 NF-kappa B binds to the DNAHIV-1 enhancer region of the long terminal repeat and contributes to the inducibility of HIV-1 gene expression in response to multiple activating agents.
2.1620 20.5275 1.0000 NF-kappa B binds to the HIV-1 enhancer region of the long terminal repeat and contributes to the inducibility of DNAHIV-1 gene expression in response to multiple activating agents.
NF-kappa B binds to the DNAHIV-1 enhancer region of the long terminal repeat and contributes to the inducibility of HIV-1 gene expression in response to multiple activating agents.
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2.1200 20.8008 1.0000 Phosphorylation and degradation of the cytoplasmic inhibitor I kappa B alpha are crucial regulatory events in the activation of proteinNF-kappa B DNA-binding activity .
3.3640 20.2071 10.5888 Phosphorylation and degradation of the cytoplasmic inhibitor proteinI kappa B alpha are crucial regulatory events in the activation of NF-kappa B DNA-binding activity .
Phosphorylation and degradation of the proteincytoplasmic inhibitor I kappa B alpha are crucial regulatory events in the activation of NF-kappa B DNA-binding activity .
Phosphorylation and degradation of the cytoplasmic inhibitor proteinI kappa B alpha are crucial regulatory events in the activation of NF-kappa B DNA-binding activity .
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4.0143 20.8224 10.5297 Both N- and C- terminal residues of proteinI kappa B alpha are required for inducer-mediated degradation .
Both N- and C- terminal residues of proteinI kappa B alpha are required for inducer-mediated degradation .
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1.6199 10.9921 1.0000 Chronic HIV-1 infection of myeloid cells leads to constitutive proteinNF-kappa B DNA-binding activity and provides an intranuclear environment capable of perpetuating HIV-1 replication .
1.5644 10.9370 0.9999 Chronic HIV-1 infection of cell_typemyeloid cells leads to constitutive NF-kappa B DNA-binding activity and provides an intranuclear environment capable of perpetuating HIV-1 replication .
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1.6184 10.4392 1.0000 Increased intracellular stores of latent proteinNF-kappa B may also result in rapid inducibility of NF-kappa B -dependent cytokine gene expression .
1.5206 10.9214 1.0000 Increased intracellular stores of latent NF-kappa B may also result in rapid inducibility of proteinNF-kappa B -dependent cytokine gene expression .
1.4813 10.9052 0.9994 Increased intracellular stores of latent NF-kappa B may also result in rapid inducibility of NF-kappa B -dependent DNAcytokine gene expression .
Increased intracellular stores of proteinlatent NF-kappa B may also result in rapid inducibility of NF-kappa B -dependent cytokine gene expression .
Increased intracellular stores of latent NF-kappa B may also result in rapid inducibility of NF-kappa B -dependent proteincytokine gene expression .
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2.1171 20.0213 0.9995 In response to secondary pathogenic infections or antigenic challenge, cytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in HIV-1 -infected myeloid cells compared with cell_typeuninfected cells .
1.4885 10.6724 0.9953 In response to secondary pathogenic infections or antigenic challenge, proteincytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in HIV-1 -infected myeloid cells compared with uninfected cells .
4.1062 20.7911 10.9808 In response to secondary pathogenic infections or antigenic challenge, cytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in cell_typeHIV-1 -infected myeloid cells compared with uninfected cells .
1.3530 10.6796 1.0000 In response to secondary pathogenic infections or antigenic challenge, DNAcytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in HIV-1 -infected myeloid cells compared with uninfected cells .
In response to secondary pathogenic infections or antigenic challenge, cytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in HIV-1 -infected cell_typemyeloid cells compared with uninfected cells .
In response to secondary pathogenic infections or antigenic challenge, cytokine gene expression is rapidly induced, enhanced, and sustained over prolonged periods in cell_lineHIV-1 -infected myeloid cells compared with uninfected cells .
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2.2097 20.4997 1.0000 Elevated levels of several proteininflammatory cytokines have been detected in the sera of HIV-1 -infected individuals .
0.8908 1.0000 1.0000 Elevated levels of several inflammatory proteincytokines have been detected in the sera of HIV-1 -infected individuals .
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2.8444 20.4381 10.8586 Secretion of proteinmyeloid cell-derived cytokines may both increase virus production and contribute to AIDS-associated disorders .
0.9291 1.0000 1.0000 Secretion of myeloid cell-derived proteincytokines may both increase virus production and contribute to AIDS-associated disorders .
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1.2963 10.9022 1.0000 Steroid mediated lysis of cell_typelymphoblasts requires the DNA binding region of the steroid hormone receptor.
3.2532 20.3493 10.8781 Steroid mediated lysis of lymphoblasts requires the proteinDNA binding region of the steroid hormone receptor.
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1.6621 10.5369 1.0000 Glucocorticoids kill certain types of cell_typelymphoblasts , but the mechanisms are unknown.
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1.7381 10.7571 1.0000 It is clear that sufficient numbers of functional proteinglucocorticoid receptors are required to mediate lysis, but whether they do so through the classical model of steroid hormone activation and modulation of gene expression has not been established.
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3.6947 20.9355 10.6753 In this report we have asked which region(s) of the steroid receptor are important for mediating lysis in cell_typeleukemic T lymphoblasts .
2.2030 20.3099 1.0000 In this report we have asked which region(s) of the proteinsteroid receptor are important for mediating lysis in leukemic T lymphoblasts .
In this report we have asked which region(s) of the steroid receptor are important for mediating lysis in leukemic T cell_typelymphoblasts .
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2.2223 20.4317 0.9999 CEM-ICR 27 leukemic lymphoblasts , a clone of cell_lineCEM cells which lack functional glucocorticoid receptors and therefore are neither lysed by dexamethasone nor capable of showing glutamine synthetase induction , were provided with steroid receptors by DNA transfections of various receptor gene constructs.
2.1912 20.3969 1.0000 CEM-ICR 27 leukemic lymphoblasts , a clone of CEM cells which lack functional glucocorticoid receptors and therefore are neither lysed by dexamethasone nor capable of showing proteinglutamine synthetase induction , were provided with steroid receptors by DNA transfections of various receptor gene constructs.
2.1193 20.8840 1.0000 CEM-ICR 27 leukemic lymphoblasts , a clone of CEM cells which lack functional proteinglucocorticoid receptors and therefore are neither lysed by dexamethasone nor capable of showing glutamine synthetase induction , were provided with steroid receptors by DNA transfections of various receptor gene constructs.
2.1144 20.7663 1.0000 CEM-ICR 27 leukemic lymphoblasts , a clone of CEM cells which lack functional glucocorticoid receptors and therefore are neither lysed by dexamethasone nor capable of showing glutamine synthetase induction , were provided with proteinsteroid receptors by DNA transfections of various receptor gene constructs.
0.8434 0.9863 0.9972 cell_lineCEM-ICR 27 leukemic lymphoblasts , a clone of CEM cells which lack functional glucocorticoid receptors and therefore are neither lysed by dexamethasone nor capable of showing glutamine synthetase induction , were provided with steroid receptors by DNA transfections of various receptor gene constructs.
CEM-ICR 27 leukemic cell_typelymphoblasts , a clone of CEM cells which lack functional glucocorticoid receptors and therefore are neither lysed by dexamethasone nor capable of showing glutamine synthetase induction , were provided with steroid receptors by DNA transfections of various receptor gene constructs.
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2.2508 20.5616 1.0000 We measured steroid mediated lysis , receptor number and induction of proteinglutamine synthetase in the transfected cells .
1.5668 10.6192 0.9998 We measured steroid mediated lysis , receptor number and induction of glutamine synthetase in the cell_linetransfected cells .
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1.8892 20.2163 1.0000 Our results provide evidence that the lysis mechanism in the cell_lineICR27 lymphoblasts is restored when functional receptor number is restored.
Our results provide evidence that the lysis mechanism in the ICR27 cell_typelymphoblasts is restored when functional receptor number is restored.
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1.4201 10.9104 1.0000 The DNA binding region specifying high affinity for DNAGRE sites is required.
2.5851 10.8305 10.5301 The DNADNA binding region specifying high affinity for GRE sites is required.
The proteinDNA binding region specifying high affinity for GRE sites is required.
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4.0253 20.8261 10.6421 Our data support the view that steroid -mediated cell death occurs by a process requiring direct interaction of proteinsteroid -receptor complexes with the genome.
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2.0614 20.5331 10.4427 Functional characterization of the murine homolog of the proteinB cell-specific coactivator BOB.1/OBF.1 .
1.6919 20.0274 0.9999 Functional characterization of the proteinmurine homolog of the B cell-specific coactivator BOB.1/OBF.1 .
0.9542 0.9999 1.0000 Functional characterization of the murine homolog of the B cell-specific coactivator proteinBOB.1/OBF.1 .
1.8053 20.4836 20.0708 Functional characterization of the murine homolog of the proteinB cell-specific coactivator BOB.1/OBF.1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3925 20.2665 10.6554 B cell-specific transcriptional promoter activity mediated by the octamer motif requires the Oct1 or Oct2 protein and additional proteinB cell-restricted cofactors .
2.0116 20.3846 1.0000 B cell-specific transcriptional promoter activity mediated by the DNAoctamer motif requires the Oct1 or Oct2 protein and additional B cell-restricted cofactors .
1.6333 0.9970 10.5978 DNAB cell-specific transcriptional promoter activity mediated by the octamer motif requires the Oct1 or Oct2 protein and additional B cell-restricted cofactors .
B cell-specific transcriptional promoter activity mediated by the octamer motif requires the proteinOct1 or Oct2 protein and additional B cell-restricted cofactors .
B cell-specific transcriptional promoter activity mediated by the octamer motif requires the Oct1 or proteinOct2 protein and additional B cell-restricted cofactors .
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3.4187 20.4599 10.6589 One such cofactor , BOB.1/OBF.1 , was recently isolated from cell_typehuman B cells .
1.6869 10.1399 1.0000 One such cofactor , proteinBOB.1/OBF.1 , was recently isolated from human B cells .
1.5728 10.7577 1.0000 One such proteincofactor , BOB.1/OBF.1 , was recently isolated from human B cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1926 20.1122 1.0000 Here, we describe the isolation and detailed characterization of the proteinmurine homolog .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6174 10.7829 1.0000 Full-length cDNAs and DNAgenomic clones were isolated, and the gene structure was determined. Comparison of the deduced amino acids shows 88% sequence identity between mouse and human BOB.1/OBF.1 .
0.9211 1.0000 1.0000 Full-length DNAcDNAs and genomic clones were isolated, and the gene structure was determined. Comparison of the deduced amino acids shows 88% sequence identity between mouse and human BOB.1/OBF.1 .
2.2066 20.6496 0.9998 Full-length cDNAs and genomic clones were isolated, and the gene structure was determined. Comparison of the deduced amino acids shows 88% sequence identity between mouse and proteinhuman BOB.1/OBF.1 .
1.4828 20.1616 1.0000 Full-length cDNAs and genomic clones were isolated, and the gene structure was determined. Comparison of the deduced proteinamino acids shows 88% sequence identity between mouse and human BOB.1/OBF.1 .
0.7313 0.9975 0.9998 DNAFull-length cDNAs and genomic clones were isolated, and the gene structure was determined. Comparison of the deduced amino acids shows 88% sequence identity between mouse and human BOB.1/OBF.1 .
0.5284 1.0000 0.9999 Full-length cDNAs and genomic clones were isolated, and the gene structure was determined. Comparison of the deduced amino acids shows 88% sequence identity between mouse and human proteinBOB.1/OBF.1 .
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3.3035 10.6109 10.9667 The proteinNH2-terminal 126 amino acids of BOB.1/OBF.1 are both essential and sufficient for interaction with the POU domains of either Oct1 or Oct2 .
1.4957 10.4001 1.0000 The NH2-terminal 126 amino acids of BOB.1/OBF.1 are both essential and sufficient for interaction with the POU domains of either proteinOct1 or Oct2 .
1.3102 10.9910 0.9999 The NH2-terminal 126 amino acids of BOB.1/OBF.1 are both essential and sufficient for interaction with the proteinPOU domains of either Oct1 or Oct2 .
0.8833 1.0000 1.0000 The NH2-terminal 126 amino acids of proteinBOB.1/OBF.1 are both essential and sufficient for interaction with the POU domains of either Oct1 or Oct2 .
0.8769 1.0000 1.0000 The NH2-terminal 126 amino acids of BOB.1/OBF.1 are both essential and sufficient for interaction with the POU domains of either Oct1 or proteinOct2 .
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2.3859 20.3017 1.0000 This protein-protein interaction does not require the simultaneous binding of proteinOct proteins to DNA, and high resolution footprinting of the Oct -DNA interaction reveals that binding of BOB.1/OBF.1 to Oct1 or Oct2 does not alter the interaction with DNA.
1.6158 10.3747 1.0000 This protein-protein interaction does not require the simultaneous binding of Oct proteins to DNA, and high resolution footprinting of the Oct -DNA interaction reveals that binding of proteinBOB.1/OBF.1 to Oct1 or Oct2 does not alter the interaction with DNA.
0.9162 1.0000 1.0000 This protein-protein interaction does not require the simultaneous binding of Oct proteins to DNA, and high resolution footprinting of the Oct -DNA interaction reveals that binding of BOB.1/OBF.1 to Oct1 or proteinOct2 does not alter the interaction with DNA.
0.8585 1.0000 1.0000 This protein-protein interaction does not require the simultaneous binding of Oct proteins to DNA, and high resolution footprinting of the Oct -DNA interaction reveals that binding of BOB.1/OBF.1 to proteinOct1 or Oct2 does not alter the interaction with DNA.
0.9127 1.0000 1.0000 This protein-protein interaction does not require the simultaneous binding of Oct proteins to DNA, and high resolution footprinting of the proteinOct -DNA interaction reveals that binding of BOB.1/OBF.1 to Oct1 or Oct2 does not alter the interaction with DNA.
This protein-protein interaction does not require the simultaneous binding of Oct proteins to DNA, and high resolution footprinting of the DNAOct -DNA interaction reveals that binding of BOB.1/OBF.1 to Oct1 or Oct2 does not alter the interaction with DNA.
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2.1275 20.7531 1.0000 BOB.1/OBF.1 can efficiently activate octamer-dependent promoters in fibroblasts ; however, it fails to stimulate DNAoctamer-dependent enhancer activity .
0.9565 1.0000 1.0000 proteinBOB.1/OBF.1 can efficiently activate octamer-dependent promoters in fibroblasts ; however, it fails to stimulate octamer-dependent enhancer activity .
0.8276 0.9999 1.0000 BOB.1/OBF.1 can efficiently activate octamer-dependent promoters in cell_typefibroblasts ; however, it fails to stimulate octamer-dependent enhancer activity .
2.1218 20.4326 1.0000 BOB.1/OBF.1 can efficiently activate DNAoctamer-dependent promoters in fibroblasts ; however, it fails to stimulate octamer-dependent enhancer activity .
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4.7807 20.8348 10.9440 Fusion of subdomains of BOB.1/OBF.1 with the proteinGAL4 DNA binding domain reveals that both NH2- and COOH- terminal domains of BOB.1/OBF.1 contribute to full transactivation function, the COOH-terminal domain is more efficient in this transactivation assay .
2.2839 20.1899 0.9999 Fusion of subdomains of BOB.1/OBF.1 with the GAL4 DNA binding domain reveals that both NH2- and COOH- terminal domains of BOB.1/OBF.1 contribute to full transactivation function, the proteinCOOH-terminal domain is more efficient in this transactivation assay .
1.7617 10.0809 1.0000 Fusion of subdomains of BOB.1/OBF.1 with the GAL4 DNA binding domain reveals that both NH2- and COOH- terminal domains of proteinBOB.1/OBF.1 contribute to full transactivation function, the COOH-terminal domain is more efficient in this transactivation assay .
1.6119 10.5865 1.0000 Fusion of subdomains of proteinBOB.1/OBF.1 with the GAL4 DNA binding domain reveals that both NH2- and COOH- terminal domains of BOB.1/OBF.1 contribute to full transactivation function, the COOH-terminal domain is more efficient in this transactivation assay .
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3.7888 20.2046 10.6719 Consistent with the failure of full-length BOB.1/OBF.1 to stimulate DNAoctamer-dependent enhancer elements in non B cells , the GAL4 fusions likewise only stimulate from a promoter-proximal position .
2.3915 10.9810 10.6605 Consistent with the failure of full-length BOB.1/OBF.1 to stimulate octamer-dependent enhancer elements in cell_typenon B cells , the GAL4 fusions likewise only stimulate from a promoter-proximal position .
1.6401 10.2787 1.0000 Consistent with the failure of full-length proteinBOB.1/OBF.1 to stimulate octamer-dependent enhancer elements in non B cells , the GAL4 fusions likewise only stimulate from a promoter-proximal position .
1.4015 10.9664 1.0000 Consistent with the failure of full-length BOB.1/OBF.1 to stimulate octamer-dependent enhancer elements in non B cells , the proteinGAL4 fusions likewise only stimulate from a promoter-proximal position .
1.3411 10.9316 0.9998 Consistent with the failure of full-length BOB.1/OBF.1 to stimulate octamer-dependent enhancer elements in non B cells , the GAL4 fusions likewise only stimulate from a DNApromoter-proximal position .
0.6194 0.9999 0.9997 Consistent with the failure of full-length BOB.1/OBF.1 to stimulate octamer-dependent enhancer elements in non cell_typeB cells , the GAL4 fusions likewise only stimulate from a promoter-proximal position .
Consistent with the failure of proteinfull-length BOB.1/OBF.1 to stimulate octamer-dependent enhancer elements in non B cells , the GAL4 fusions likewise only stimulate from a promoter-proximal position .
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3.6608 10.6713 20.2647 Anti-immunoglobulin M activates proteinnuclear calcium/calmodulin-dependent protein kinase II in human B lymphocytes .
2.5637 20.8514 10.8305 Anti-immunoglobulin M activates nuclear calcium/calmodulin-dependent protein kinase II in cell_typehuman B lymphocytes .
0.7461 0.9981 0.9993 proteinAnti-immunoglobulin M activates nuclear calcium/calmodulin-dependent protein kinase II in human B lymphocytes .
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3.8786 20.8391 10.2988 We and others have previously shown that the nuclear protein , Ets-1 , is phosphorylated in a calcium-dependent manner after ligation of proteinimmunoglobulin (Ig) M on B lymphocytes .
2.2858 20.1737 1.0000 We and others have previously shown that the proteinnuclear protein , Ets-1 , is phosphorylated in a calcium-dependent manner after ligation of immunoglobulin (Ig) M on B lymphocytes .
1.5196 10.5954 0.9995 We and others have previously shown that the nuclear protein , Ets-1 , is phosphorylated in a calcium-dependent manner after ligation of immunoglobulin (Ig) M on cell_typeB lymphocytes .
0.9411 1.0000 1.0000 We and others have previously shown that the nuclear protein , proteinEts-1 , is phosphorylated in a calcium-dependent manner after ligation of immunoglobulin (Ig) M on B lymphocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7268 20.9744 10.9026 As this phosphorylation was independent of protein kinase C activity , we tested whether a proteincalcium/calmodulin-dependent protein kinase ( CaM kinase ) might phosphorylate the Ets-1 protein after elevation of intracellular free calcium concentrations .
3.5558 20.9711 10.9876 As this phosphorylation was independent of proteinprotein kinase C activity , we tested whether a calcium/calmodulin-dependent protein kinase ( CaM kinase ) might phosphorylate the Ets-1 protein after elevation of intracellular free calcium concentrations .
2.0505 20.8416 1.0000 As this phosphorylation was independent of protein kinase C activity , we tested whether a calcium/calmodulin-dependent protein kinase ( CaM kinase ) might phosphorylate the proteinEts-1 protein after elevation of intracellular free calcium concentrations .
1.8887 20.9119 0.9892 As this phosphorylation was independent of protein kinase C activity , we tested whether a calcium/calmodulin-dependent protein kinase ( CaM kinase ) might phosphorylate the proteinEts-1 protein after elevation of intracellular free calcium concentrations .
1.6640 10.0202 1.0000 As this phosphorylation was independent of protein kinase C activity , we tested whether a calcium/calmodulin-dependent protein kinase ( proteinCaM kinase ) might phosphorylate the Ets-1 protein after elevation of intracellular free calcium concentrations .
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1.7715 10.9453 1.0000 The dephosphorylated form of Ets-1 has been shown to bind to DNAchromatin , suggesting that the operative kinase should be detectable in the nucleus .
1.6830 10.6451 1.0000 The dephosphorylated form of proteinEts-1 has been shown to bind to chromatin , suggesting that the operative kinase should be detectable in the nucleus .
The dephosphorylated form of Ets-1 has been shown to bind to chromatin , suggesting that the proteinoperative kinase should be detectable in the nucleus .
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4.0684 20.9953 10.8758 We prepared nuclear extracts from two cell_linehuman B cell lines in which increased intracellular free calcium levels correlated with increased phosphorylation of the Ets-1 protein.
1.9889 20.6805 0.9996 We prepared nuclear extracts from two human B cell lines in which increased intracellular free calcium levels correlated with increased phosphorylation of the proteinEts-1 protein.
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3.8510 20.9928 10.4250 Activity of the CaM kinases was determined using a synthetic peptide substrate both in the absence and presence of an inhibitor specific for the proteinCaM kinase family , KN-62 .
2.2270 20.6331 1.0000 Activity of the proteinCaM kinases was determined using a synthetic peptide substrate both in the absence and presence of an inhibitor specific for the CaM kinase family , KN-62 .
2.1792 20.9616 10.5753 Activity of the CaM kinases was determined using a proteinsynthetic peptide substrate both in the absence and presence of an inhibitor specific for the CaM kinase family , KN-62 .
0.8316 0.9999 1.0000 Activity of the CaM kinases was determined using a synthetic peptide substrate both in the absence and presence of an inhibitor specific for the CaM kinase family , proteinKN-62 .
Activity of the CaM kinases was determined using a synthetic peptide substrate both in the absence and presence of an inhibitor specific for the proteinCaM kinase family , KN-62 .
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2.4160 20.1691 1.0000 Stimulation of cells with anti-IgM led to increased activity of a proteinnuclear kinase that could phosphorylate the peptide, and this activity was reduced by 10 microM KN-62 .
1.7580 10.7099 1.0000 Stimulation of cells with proteinanti-IgM led to increased activity of a nuclear kinase that could phosphorylate the peptide, and this activity was reduced by 10 microM KN-62 .
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2.9084 20.7231 10.6262 Kinase activity was reduced in lysates preadsorbed using an antibody specific for proteinCaM kinase II .
Kinase activity was reduced in lysates preadsorbed using an proteinantibody specific for CaM kinase II .
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1.6960 10.3552 1.0000 Two-dimensional phosphopeptide maps of the Ets-1 protein from cells incubated with ionomycin or proteinanti-IgM contained two unique phosphopeptides that were absent in untreated cells.
1.4612 10.7877 1.0000 Two-dimensional phosphopeptide maps of the proteinEts-1 protein from cells incubated with ionomycin or anti-IgM contained two unique phosphopeptides that were absent in untreated cells.
0.9168 1.0000 1.0000 Two-dimensional phosphopeptide maps of the Ets-1 protein from cells incubated with ionomycin or anti-IgM contained two unique proteinphosphopeptides that were absent in untreated cells.
Two-dimensional phosphopeptide maps of the proteinEts-1 protein from cells incubated with ionomycin or anti-IgM contained two unique phosphopeptides that were absent in untreated cells.
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3.4565 20.4599 10.7863 Incubation of isolated Ets-1 protein with purified proteinCaM kinase II produced phosphorylation of peptides that migrated identically to those found in cells incubated with either anti-IgM or ionomycin .
1.5603 10.6995 1.0000 Incubation of isolated Ets-1 protein with purified CaM kinase II produced phosphorylation of peptides that migrated identically to those found in cells incubated with either proteinanti-IgM or ionomycin .
1.9877 20.9442 0.9999 Incubation of isolated proteinEts-1 protein with purified CaM kinase II produced phosphorylation of peptides that migrated identically to those found in cells incubated with either anti-IgM or ionomycin .
Incubation of proteinisolated Ets-1 protein with purified CaM kinase II produced phosphorylation of peptides that migrated identically to those found in cells incubated with either anti-IgM or ionomycin .
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5.5454 30.1832 10.5425 These data suggest a model of signal transduction by the antigen receptor on B lymphocytes in which increased intracellular free calcium can rapidly activate proteinnuclear CaM kinase II , potentially resulting in phosphorylation and regulation of DNA-binding proteins .
2.1644 20.6043 0.9999 These data suggest a model of signal transduction by the proteinantigen receptor on B lymphocytes in which increased intracellular free calcium can rapidly activate nuclear CaM kinase II , potentially resulting in phosphorylation and regulation of DNA-binding proteins .
2.1639 20.4714 0.9999 These data suggest a model of signal transduction by the antigen receptor on B lymphocytes in which increased intracellular free calcium can rapidly activate nuclear CaM kinase II , potentially resulting in phosphorylation and regulation of proteinDNA-binding proteins .
1.5184 10.8849 0.9998 These data suggest a model of signal transduction by the antigen receptor on cell_typeB lymphocytes in which increased intracellular free calcium can rapidly activate nuclear CaM kinase II , potentially resulting in phosphorylation and regulation of DNA-binding proteins .
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3.4206 20.7943 10.8612 Transcriptional activation and repression , two properties of the proteinlymphoid-specific transcription factor Oct-2a .
0.9833 1.0000 1.0000 Transcriptional activation and repression , two properties of the lymphoid-specific transcription factor proteinOct-2a .
0.6191 0.9999 0.9950 Transcriptional activation and repression , two properties of the lymphoid-specific proteintranscription factor Oct-2a .
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3.2897 20.8252 10.7515 The lymphoid-specific transcription factor Oct-2a contains two proteintranscriptional activation domains which are located within the N-terminal and C-terminal regions .
2.8167 10.5730 10.5264 The proteinlymphoid-specific transcription factor Oct-2a contains two transcriptional activation domains which are located within the N-terminal and C-terminal regions .
0.9858 1.0000 1.0000 The lymphoid-specific transcription factor proteinOct-2a contains two transcriptional activation domains which are located within the N-terminal and C-terminal regions .
The lymphoid-specific transcription factor Oct-2a contains two transcriptional activation domains which are located within the proteinN-terminal and C-terminal regions .
The lymphoid-specific transcription factor Oct-2a contains two transcriptional activation domains which are located within the N-terminal and proteinC-terminal regions .
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2.8001 20.2904 10.8497 To study their differential activation properties , we linked the isolated effector domains to the proteinGAL4 DNA-binding domain .
2.0304 20.1604 0.9999 To study their differential activation properties , we linked the isolated proteineffector domains to the GAL4 DNA-binding domain .
To study their proteindifferential activation properties , we linked the isolated effector domains to the GAL4 DNA-binding domain .
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2.3160 20.1513 1.0000 We have shown that both activating regions of Oct-2a , isolated from their natural context, can activate transcription as proteinpromoter factors .
1.7376 10.2437 1.0000 We have shown that both activating regions of proteinOct-2a , isolated from their natural context, can activate transcription as promoter factors .
2.2976 20.0770 1.0000 We have shown that both proteinactivating regions of Oct-2a , isolated from their natural context, can activate transcription as promoter factors .
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3.8826 20.8306 10.4568 In contrast to the C-terminus , activation by the N-terminal domain is dependent on a yet unidentified factor(s) binding to the DNAsimian virus 40 enhancer .
2.0948 20.2882 1.0000 In contrast to the C-terminus , activation by the proteinN-terminal domain is dependent on a yet unidentified factor(s) binding to the simian virus 40 enhancer .
1.4555 10.5934 1.0000 In contrast to the proteinC-terminus , activation by the N-terminal domain is dependent on a yet unidentified factor(s) binding to the simian virus 40 enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4635 20.1464 1.0000 The results obtained by duplication of proteinactivation domains or their mixed combination suggest that the domains are functionally independent.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6743 10.2644 0.9998 However, activation from a remote position could only be achieved with the C-terminus of Oct-2a in cell_typeB cells .
1.5726 10.6212 1.0000 However, activation from a remote position could only be achieved with the proteinC-terminus of Oct-2a in B cells .
0.8378 0.9999 1.0000 However, activation from a remote position could only be achieved with the C-terminus of proteinOct-2a in B cells .
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2.2549 20.5740 1.0000 In lymphoid cells , higher activation levels were observed, suggesting that distinct proteinB-cell-specific cofactors in concert with the effector domains of Oct-2a might be involved in mediating transcription from proximal and remote positions .
2.2524 20.6411 1.0000 In lymphoid cells , higher activation levels were observed, suggesting that distinct B-cell-specific cofactors in concert with the proteineffector domains of Oct-2a might be involved in mediating transcription from proximal and remote positions .
1.7604 10.2983 1.0000 In lymphoid cells , higher activation levels were observed, suggesting that distinct B-cell-specific cofactors in concert with the effector domains of proteinOct-2a might be involved in mediating transcription from proximal and remote positions .
1.6225 10.1449 0.9999 In cell_typelymphoid cells , higher activation levels were observed, suggesting that distinct B-cell-specific cofactors in concert with the effector domains of Oct-2a might be involved in mediating transcription from proximal and remote positions .
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0.8085 0.9999 1.0000 Furthermore, we identified a repression domain at the N-terminus of proteinOct-2a .
2.0013 20.4431 0.9999 Furthermore, we identified a proteinrepression domain at the N-terminus of Oct-2a .
1.1503 10.9774 0.9999 Furthermore, we identified a repression domain at the proteinN-terminus of Oct-2a .
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2.3276 20.3442 1.0000 When transferred to a proteinpotent activator , transcriptional stimulation was inhibited efficiently.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7318 10.6821 1.0000 These results underscore the modular structure of proteinOct-2a with separable domains for activation and repression and suggest that Oct-2a might have complex regulatory functions in vivo.
1.7166 10.5576 1.0000 These results underscore the modular structure of Oct-2a with separable domains for activation and repression and suggest that proteinOct-2a might have complex regulatory functions in vivo.
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1.7292 10.3694 1.0000 Nonopsonic phagocytosis of Pseudomonas aeruginosa by cell_typemacrophages and polymorphonuclear leukocytes requires the presence of the bacterial flagellum .
1.5671 10.3535 0.9999 Nonopsonic phagocytosis of Pseudomonas aeruginosa by macrophages and cell_typepolymorphonuclear leukocytes requires the presence of the bacterial flagellum .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6011 20.7191 10.3767 To identify the requisite bacterial ligands , studies with isogenic mutants of P. aeruginosa PAK lacking pili , flagella , and the proteinRpoN sigma factor were undertaken.
3.5010 20.4506 10.7673 To identify the requisite bacterial ligands , studies with isogenic mutants of proteinP. aeruginosa PAK lacking pili , flagella , and the RpoN sigma factor were undertaken.
1.5216 20.0733 0.9949 To identify the requisite bacterial ligands , studies with isogenic mutants of P. aeruginosa PAK lacking pili , flagella , and the proteinRpoN sigma factor were undertaken.
0.9615 1.0000 1.0000 To identify the requisite bacterial ligands , studies with isogenic mutants of P. aeruginosa PAK lacking pili , proteinflagella , and the RpoN sigma factor were undertaken.
0.9550 1.0000 1.0000 To identify the requisite bacterial ligands , studies with isogenic mutants of P. aeruginosa PAK lacking proteinpili , flagella , and the RpoN sigma factor were undertaken.
0.7312 1.0000 1.0000 To identify the requisite bacterial ligands , studies with isogenic mutants of P. aeruginosa proteinPAK lacking pili , flagella , and the RpoN sigma factor were undertaken.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5200 10.5764 0.9999 The RpoN mutant , lacking pili , flagella , and nonpilus adhesins , bound poorly and was resistant to ingestion by both cell_typemacrophages and neutrophils .
1.4791 10.6749 0.9999 The RpoN mutant , lacking pili , flagella , and proteinnonpilus adhesins , bound poorly and was resistant to ingestion by both macrophages and neutrophils .
0.8422 0.9999 0.9999 The RpoN mutant , lacking pili , flagella , and nonpilus adhesins , bound poorly and was resistant to ingestion by both macrophages and cell_typeneutrophils .
1.6827 10.9191 1.0000 The RpoN mutant , lacking proteinpili , flagella , and nonpilus adhesins , bound poorly and was resistant to ingestion by both macrophages and neutrophils .
1.5543 10.5255 0.9866 The proteinRpoN mutant , lacking pili , flagella , and nonpilus adhesins , bound poorly and was resistant to ingestion by both macrophages and neutrophils .
1.4217 10.7077 1.0000 The proteinRpoN mutant , lacking pili , flagella , and nonpilus adhesins , bound poorly and was resistant to ingestion by both macrophages and neutrophils .
0.9395 1.0000 1.0000 The RpoN mutant , lacking pili , proteinflagella , and nonpilus adhesins , bound poorly and was resistant to ingestion by both macrophages and neutrophils .
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0.9861 1.0000 1.0000 proteinPili were not absolutely required for binding or phagocytosis of P. aeruginosa .
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1.9047 10.1228 1.0000 The presence of a flagellum was not required for binding of P. aeruginosa to cell_typemacrophages but was critical for the subsequent internalization of the bacterium , suggesting that this factor or a surface ligand associated with its assembly was responsible for stimulation of nonopsonic phagocytosis .
2.5270 20.3615 1.0000 The presence of a flagellum was not required for binding of P. aeruginosa to macrophages but was critical for the subsequent internalization of the bacterium , suggesting that this factor or a proteinsurface ligand associated with its assembly was responsible for stimulation of nonopsonic phagocytosis .
0.9294 1.0000 1.0000 The presence of a proteinflagellum was not required for binding of P. aeruginosa to macrophages but was critical for the subsequent internalization of the bacterium , suggesting that this factor or a surface ligand associated with its assembly was responsible for stimulation of nonopsonic phagocytosis .
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4.9402 20.9445 10.5430 Identification of essential GATA and Ets binding motifs within the promoter of the DNAplatelet glycoprotein Ib alpha gene .
1.6220 20.7177 10.5157 Identification of essential GATA and Ets binding motifs within the promoter of the proteinplatelet glycoprotein Ib alpha gene .
0.8494 1.0000 1.0000 Identification of essential GATA and Ets binding motifs within the DNApromoter of the platelet glycoprotein Ib alpha gene .
Identification of essential GATA and DNAEts binding motifs within the promoter of the platelet glycoprotein Ib alpha gene .
Identification of essential DNAGATA and Ets binding motifs within the promoter of the platelet glycoprotein Ib alpha gene .
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4.1592 30.4002 10.4774 Platelet glycoprotein ( GP ) Ib-IX-V is a proteinmultisubunit adhesion receptor that supports platelet attachment to thrombogenic surfaces at sites of vascular injury .
1.7152 0.9983 20.9867 proteinPlatelet glycoprotein ( GP ) Ib-IX-V is a multisubunit adhesion receptor that supports platelet attachment to thrombogenic surfaces at sites of vascular injury .
proteinPlatelet glycoprotein ( GP ) Ib-IX-V is a multisubunit adhesion receptor that supports platelet attachment to thrombogenic surfaces at sites of vascular injury .
Platelet glycoprotein ( GP ) proteinIb-IX-V is a multisubunit adhesion receptor that supports platelet attachment to thrombogenic surfaces at sites of vascular injury .
Platelet glycoprotein ( proteinGP ) Ib-IX-V is a multisubunit adhesion receptor that supports platelet attachment to thrombogenic surfaces at sites of vascular injury .
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2.3593 20.4433 1.0000 The congenital absence of the receptor results in a bleeding disorder associated with cell_type"giant" platelets , a condition linking the expression of the complex to platelet morphogenesis .
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3.8921 20.5679 10.3703 To understand better the expression of the GP Ib-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the alpha-subunit of the complex ( proteinGP Ib alpha ).
3.8846 20.9111 10.6199 To understand better the expression of the proteinGP Ib-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the alpha-subunit of the complex ( GP Ib alpha ).
1.5628 10.1821 1.0000 To understand better the expression of the GP Ib-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the proteinalpha-subunit of the complex ( GP Ib alpha ).
0.7211 0.9999 1.0000 To understand better the expression of the GP Ib-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the alpha-subunit of the proteincomplex ( GP Ib alpha ).
To understand better the expression of the GP proteinIb-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the alpha-subunit of the complex ( GP Ib alpha ).
To understand better the expression of the proteinGP Ib-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the alpha-subunit of the complex ( GP Ib alpha ).
To understand better the expression of the GP Ib-IX-V complex , studies were undertaken to define the essential DNAgenetic elements supporting the expression of the alpha-subunit of the complex ( GP Ib alpha ).
To understand better the expression of the GP Ib-IX-V complex , studies were undertaken to define the essential genetic elements supporting the expression of the alpha-subunit of the complex ( proteinGP Ib alpha ).
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0.8788 1.0000 1.0000 GP Ib alpha promoter activity was evaluated by transfection of human erythroleukemia cells with reporter plasmids coding for the enzyme , proteinluciferase .
3.7895 20.5507 10.6806 GP Ib alpha promoter activity was evaluated by transfection of cell_linehuman erythroleukemia cells with reporter plasmids coding for the enzyme , luciferase .
1.5813 0.9995 10.8829 proteinGP Ib alpha promoter activity was evaluated by transfection of human erythroleukemia cells with reporter plasmids coding for the enzyme , luciferase .
1.4441 10.4605 0.9999 GP Ib alpha promoter activity was evaluated by transfection of human erythroleukemia cells with DNAreporter plasmids coding for the enzyme , luciferase .
0.7766 0.9996 0.9999 GP Ib alpha DNApromoter activity was evaluated by transfection of human erythroleukemia cells with reporter plasmids coding for the enzyme , luciferase .
proteinGP Ib alpha promoter activity was evaluated by transfection of human erythroleukemia cells with reporter plasmids coding for the enzyme , luciferase .
GP Ib alpha promoter activity was evaluated by transfection of human erythroleukemia cells with reporter plasmids coding for the proteinenzyme , luciferase .
GP Ib alpha promoter activity was evaluated by transfection of cell_typehuman erythroleukemia cells with reporter plasmids coding for the enzyme , luciferase .
DNAGP Ib alpha promoter activity was evaluated by transfection of human erythroleukemia cells with reporter plasmids coding for the enzyme , luciferase .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6193 20.3441 10.6941 Studies were initiated with a fragment extending 2,738 nucleotides 5' to the DNAtranscription start site and lead to the identification of 253 nucleotides retaining full promoter activity in human erythroleukemia cells .
3.4799 20.3202 10.7167 Studies were initiated with a fragment extending 2,738 nucleotides 5' to the transcription start site and lead to the identification of 253 nucleotides retaining full promoter activity in cell_typehuman erythroleukemia cells .
2.1261 20.8576 1.0000 Studies were initiated with a fragment extending 2,738 nucleotides 5' to the transcription start site and lead to the identification of DNA253 nucleotides retaining full promoter activity in human erythroleukemia cells .
1.7647 20.7815 0.9871 Studies were initiated with a fragment extending DNA2,738 nucleotides 5' to the transcription start site and lead to the identification of 253 nucleotides retaining full promoter activity in human erythroleukemia cells .
1.3780 20.6004 0.9999 Studies were initiated with a fragment extending DNA2,738 nucleotides 5' to the transcription start site and lead to the identification of 253 nucleotides retaining full promoter activity in human erythroleukemia cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3652 20.8754 10.9338 In cells of nonhematopoietic lineage , human endothelial and HeLa cells , the proteinGP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
2.1716 20.6791 0.9999 In cells of nonhematopoietic lineage , human endothelial and HeLa cells , the GP Ib alpha promoter activity was no greater than background levels obtained with DNApromoterless constructs .
1.2408 10.9233 0.9998 In cells of cell_typenonhematopoietic lineage , human endothelial and HeLa cells , the GP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
1.1679 10.4532 0.9998 In cells of nonhematopoietic lineage , cell_typehuman endothelial and HeLa cells , the GP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
1.5062 10.9910 0.9999 In cells of nonhematopoietic lineage , human endothelial and cell_lineHeLa cells , the GP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
In cells of nonhematopoietic lineage , human endothelial and HeLa cells , the proteinGP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
In cells of nonhematopoietic lineage , human endothelial and HeLa cells , the DNAGP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
In cells of nonhematopoietic lineage , human endothelial and cell_typeHeLa cells , the GP Ib alpha promoter activity was no greater than background levels obtained with promoterless constructs .
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4.0003 20.8275 10.8839 Gel shift assays and site-directed mutagenesis studies defined essential GATA and Ets binding motifs 93 and 150 nucleotides upstream of the DNAtranscription start site , a finding which further substantiates these elements as important determinants of megakaryocytic gene expression .
1.3755 10.5770 0.9999 Gel shift assays and site-directed mutagenesis studies defined essential GATA and Ets binding motifs 93 and 150 nucleotides upstream of the transcription start site , a finding which further substantiates these elements as important determinants of DNAmegakaryocytic gene expression .
Gel shift assays and site-directed mutagenesis studies defined essential DNAGATA and Ets binding motifs 93 and 150 nucleotides upstream of the transcription start site , a finding which further substantiates these elements as important determinants of megakaryocytic gene expression .
Gel shift assays and site-directed mutagenesis studies defined essential GATA and DNAEts binding motifs 93 and 150 nucleotides upstream of the transcription start site , a finding which further substantiates these elements as important determinants of megakaryocytic gene expression .
Gel shift assays and site-directed mutagenesis studies defined essential GATA and Ets binding motifs DNA93 and 150 nucleotides upstream of the transcription start site , a finding which further substantiates these elements as important determinants of megakaryocytic gene expression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8383 20.7992 10.5505 The results define essential cis-acting elements responsible for the expression of proteinGP Ib alpha and provide insights into molecular events coinciding with the release of normal platelets into the bloodstream .
2.2835 20.8047 0.9999 The results define essential cis-acting elements responsible for the expression of GP Ib alpha and provide insights into molecular events coinciding with the release of cell_typenormal platelets into the bloodstream .
2.1532 20.6070 0.9999 The results define essential DNAcis-acting elements responsible for the expression of GP Ib alpha and provide insights into molecular events coinciding with the release of normal platelets into the bloodstream .
The results define essential cis-acting elements responsible for the expression of proteinGP Ib alpha and provide insights into molecular events coinciding with the release of normal platelets into the bloodstream .
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3.6039 20.1251 10.7102 CD30 ligation induces nuclear factor-kappa B activation in cell_linehuman T cell lines .
3.0375 20.5739 10.5746 CD30 ligation induces proteinnuclear factor-kappa B activation in human T cell lines .
0.9633 1.0000 1.0000 proteinCD30 ligation induces nuclear factor-kappa B activation in human T cell lines .
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6.2371 30.5382 20.2304 CD30 is a recently described member of the proteintumor necrosis factor /nerve growth factor receptor superfamily .
0.9541 1.0000 1.0000 proteinCD30 is a recently described member of the tumor necrosis factor /nerve growth factor receptor superfamily .
CD30 is a recently described member of the tumor necrosis factor protein/nerve growth factor receptor superfamily .
CD30 is a recently described member of the proteintumor necrosis factor /nerve growth factor receptor superfamily .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7043 20.8546 20.6151 In this report, we show that following incubation of L540 cells ( cell_lineHodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( mAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
4.6599 20.6734 10.9177 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( mAb ) M44 and M67 , two proteinnuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
1.4059 10.9800 0.9992 In this report, we show that following incubation of cell_lineL540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( mAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
0.9715 1.0000 0.9837 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, proteinCD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( mAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
0.9644 1.0000 1.0000 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( proteinmAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
0.9633 1.0000 1.0000 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( mAb ) proteinM44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
0.9632 1.0000 1.0000 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- CD30 monoclonal antibodies ( mAb ) M44 and proteinM67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
0.9348 1.0000 0.9964 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic anti- proteinCD30 monoclonal antibodies ( mAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
4.5850 20.4387 10.9107 In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the agonistic proteinanti- CD30 monoclonal antibodies ( mAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
In this report, we show that following incubation of L540 cells ( Hodgkin's disease -derived, T cell-like, CD30 + cells ) with the proteinagonistic anti- CD30 monoclonal antibodies ( mAb ) M44 and M67 , two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts , as determined in gel retardation assays .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7331 10.0295 1.0000 The effect of the mAb towards proteinNF-kappa B activation was rapid, as it occurred within 20 min, and was sustained for up to 6 h.
0.8795 0.9999 1.0000 The effect of the proteinmAb towards NF-kappa B activation was rapid, as it occurred within 20 min, and was sustained for up to 6 h.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1572 20.1493 1.0000 By comparison, an proteinisotype-matched antibody had no effect on NF-kappa B activation .
1.4696 10.9381 1.0000 By comparison, an isotype-matched antibody had no effect on proteinNF-kappa B activation .
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4.9328 20.9304 20.4660 Moreover, in cell_linehuman T helper (Th) clones functionally characterized as being of the type 0, type 1 and type 2 (28%, < 1% und 93% CD30+, respectively), the extent of CD30 -mediated NF-kappa B activation correlated with the proportion of CD30+ cells .
1.5769 10.0904 1.0000 Moreover, in human T helper (Th) clones functionally characterized as being of the type 0, type 1 and type 2 (28%, < 1% und 93% CD30+, respectively), the extent of proteinCD30 -mediated NF-kappa B activation correlated with the proportion of CD30+ cells .
1.5353 10.2926 1.0000 Moreover, in human T helper (Th) clones functionally characterized as being of the type 0, type 1 and type 2 (28%, < 1% und 93% CD30+, respectively), the extent of CD30 -mediated proteinNF-kappa B activation correlated with the proportion of CD30+ cells .
Moreover, in human T helper (Th) clones functionally characterized as being of the type 0, type 1 and type 2 (28%, < 1% und 93% CD30+, respectively), the extent of CD30 -mediated NF-kappa B activation correlated with the proportion of cell_lineCD30+ cells .
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2.2834 20.2521 0.9999 In all cell lines investigated, the proteinNF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , p65 RelA , and possibly other transcription factors .
2.0812 20.6063 0.9999 In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , p65 RelA , and possibly other proteintranscription factors .
1.8132 10.0469 1.0000 In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , proteinp65 RelA , and possibly other transcription factors .
1.7625 20.6328 0.7076 In all cell lines investigated, the proteinNF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , p65 RelA , and possibly other transcription factors .
0.8310 1.0000 1.0000 In all cell lines investigated, the NF-kappa B complexes induced following proteinCD30 engagement were shown to contain p50 NF-kappa B1 , p65 RelA , and possibly other transcription factors .
1.9679 20.0272 0.9998 In all cell_linecell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , p65 RelA , and possibly other transcription factors .
1.4654 10.0789 1.0000 In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain proteinp50 NF-kappa B1 , p65 RelA , and possibly other transcription factors .
0.8886 0.9985 1.0000 In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 proteinNF-kappa B1 , p65 RelA , and possibly other transcription factors .
0.7996 1.0000 0.9980 In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , proteinp65 RelA , and possibly other transcription factors .
0.6464 1.0000 1.0000 In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1 , p65 proteinRelA , and possibly other transcription factors .
In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain proteinp50 NF-kappa B1 , p65 RelA , and possibly other transcription factors .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4596 20.1738 1.0000 Collectively, our results demonstrate that nuclear translocation and activation of proteinNF-kappa B rank among the short-term cellular responses elicited following CD30 ligation .
1.7009 10.4515 1.0000 Collectively, our results demonstrate that nuclear translocation and activation of NF-kappa B rank among the short-term cellular responses elicited following proteinCD30 ligation .
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
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3.4193 30.9222 10.7621 This chronic inflammatory reaction results from a sequence of events that begins with the trapping of proteinlow density lipoprotein ( LDL ) in the subendothelial space of the artery wall .
3.1594 30.9078 10.9784 This chronic inflammatory reaction results from a sequence of events that begins with the trapping of proteinlow density lipoprotein ( LDL ) in the subendothelial space of the artery wall .
0.9781 1.0000 0.9891 This chronic inflammatory reaction results from a sequence of events that begins with the trapping of low density lipoprotein ( proteinLDL ) in the subendothelial space of the artery wall .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.5415 20.3371 0.9999 The trapped LDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of NFkB-like transcription factors that cause the expression of genes whose protein products mediate monocyte binding , monocyte chemotaxis into the subendothelial space , and conversion into cell_typemacrophages .
2.4402 20.6296 1.0000 The trapped LDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of NFkB-like transcription factors that cause the expression of genes whose proteinprotein products mediate monocyte binding , monocyte chemotaxis into the subendothelial space , and conversion into macrophages .
1.6304 40.9969 0.9999 The trapped LDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of proteinNFkB-like transcription factors that cause the expression of genes whose protein products mediate monocyte binding , monocyte chemotaxis into the subendothelial space , and conversion into macrophages .
2.7651 30.0401 0.9977 The trapped LDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the proteinLDL particle. Some of the lipids that result lead to the activation of NFkB-like transcription factors that cause the expression of genes whose protein products mediate monocyte binding , monocyte chemotaxis into the subendothelial space , and conversion into macrophages .
1.7650 10.3867 1.0000 The trapped proteinLDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of NFkB-like transcription factors that cause the expression of genes whose protein products mediate monocyte binding , monocyte chemotaxis into the subendothelial space , and conversion into macrophages .
The trapped LDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of NFkB-like transcription factors that cause the expression of genes whose protein products mediate monocyte binding , cell_typemonocyte chemotaxis into the subendothelial space , and conversion into macrophages .
The trapped LDL is seeded with oxidative species released by the overlying endothelium , and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of NFkB-like proteintranscription factors that cause the expression of genes whose protein products mediate monocyte binding , monocyte chemotaxis into the subendothelial space , and conversion into macrophages .
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1.6094 10.0317 1.0000 At least 1 DNAmajor gene modulates the oxidation of LDL lipids and/or the biologic response to these lipids.
0.8795 1.0000 1.0000 At least 1 major gene modulates the oxidation of proteinLDL lipids and/or the biologic response to these lipids.
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2.2588 20.2102 1.0000 The inverse relation between high density lipoprotein ( HDL ) and atherosclerotic events may in part be due to enzymes associated with HDL that destroy the biologically active lipids generated in proteinLDL .
1.7208 10.9641 1.0000 The inverse relation between high density lipoprotein ( HDL ) and atherosclerotic events may in part be due to enzymes associated with proteinHDL that destroy the biologically active lipids generated in LDL .
1.5019 30.5998 0.9999 The inverse relation between proteinhigh density lipoprotein ( HDL ) and atherosclerotic events may in part be due to enzymes associated with HDL that destroy the biologically active lipids generated in LDL .
0.9490 1.0000 1.0000 The inverse relation between high density lipoprotein ( proteinHDL ) and atherosclerotic events may in part be due to enzymes associated with HDL that destroy the biologically active lipids generated in LDL .
The inverse relation between high density lipoprotein ( HDL ) and atherosclerotic events may in part be due to proteinenzymes associated with HDL that destroy the biologically active lipids generated in LDL .
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1.5240 10.9757 1.0000 Estrogen and proteinprogesterone receptors in vernal keratoconjunctivitis .
proteinEstrogen and progesterone receptors in vernal keratoconjunctivitis .
Cls_Score Left_Reg_Score Right_Reg_Score Text
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1.6932 10.4707 1.0000 METHODS: The authors evaluated tarsal and bulbar conjunctival biopsies from seven patients with severe and symptomatic VKC for the presence of estrogen and proteinprogesterone receptors by using monoclonal antibodies with a peroxidase-antiperoxidase technique .
1.6590 10.9153 1.0000 METHODS: The authors evaluated tarsal and bulbar conjunctival biopsies from seven patients with severe and symptomatic VKC for the presence of estrogen and progesterone receptors by using proteinmonoclonal antibodies with a peroxidase-antiperoxidase technique .
0.9076 1.0000 1.0000 METHODS: The authors evaluated tarsal and bulbar conjunctival biopsies from seven patients with severe and symptomatic VKC for the presence of proteinestrogen and progesterone receptors by using monoclonal antibodies with a peroxidase-antiperoxidase technique .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.8750 0.9978 1.0000 RESULTS: Both the epithelium and subepithelium of the tarsal and bulbar conjunctiva of patients with VKC , but not those of four nonatopic control subjects , showed intense positive staining for estrogen and proteinprogesterone receptors .
0.8495 1.0000 1.0000 RESULTS: Both the epithelium and subepithelium of the tarsal and bulbar conjunctiva of patients with VKC , but not those of four nonatopic control subjects , showed intense positive staining for proteinestrogen and progesterone receptors .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0397 20.0029 10.4271 Immunofluorescence colocalization of both estrogen and progesterone receptors with proteineosinophil cationic protein showed that approximately 70% of positive cells were eosinophils .
1.5743 10.5508 0.9999 Immunofluorescence colocalization of both estrogen and progesterone receptors with eosinophil cationic protein showed that approximately 70% of positive cells were cell_typeeosinophils .
1.4471 10.3904 0.9999 Immunofluorescence colocalization of both estrogen and proteinprogesterone receptors with eosinophil cationic protein showed that approximately 70% of positive cells were eosinophils .
0.7315 1.0000 1.0000 Immunofluorescence colocalization of both proteinestrogen and progesterone receptors with eosinophil cationic protein showed that approximately 70% of positive cells were eosinophils .
Immunofluorescence colocalization of both estrogen and progesterone receptors with eosinophil cationic protein showed that approximately 70% of cell_typepositive cells were eosinophils .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6463 10.8350 1.0000 CONCLUSIONS: Sexual hormones , through their receptors , may influence the activity of cell_typeeosinophils in patients with VKC .
1.6424 10.2783 1.0000 CONCLUSIONS: Sexual hormones , through their proteinreceptors , may influence the activity of eosinophils in patients with VKC .
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3.6580 20.4718 10.8115 CIITA activates the expression of DNAMHC class II genes in mouse T cells.
0.9562 1.0000 1.0000 proteinCIITA activates the expression of MHC class II genes in mouse T cells.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.3448 30.1758 10.8947 It has long been a puzzle that MHC class II molecules are expressed in human T cells after activation but not in cell_typemouse T cells ; this expression is believed to play a role in the cell mediated immune response .
4.0555 30.0536 10.6963 It has long been a puzzle that proteinMHC class II molecules are expressed in human T cells after activation but not in mouse T cells ; this expression is believed to play a role in the cell mediated immune response .
3.5487 20.7743 10.7916 It has long been a puzzle that MHC class II molecules are expressed in cell_typehuman T cells after activation but not in mouse T cells ; this expression is believed to play a role in the cell mediated immune response .
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4.6120 30.5368 10.6630 Recently the MHC class II transactivator ( CIITA ) has been reported to be a major regulatory factor for both the constitutive and IFN inducible expression of DNAMHC class II genes .
2.5138 20.9874 10.5724 Recently the proteinMHC class II transactivator ( CIITA ) has been reported to be a major regulatory factor for both the constitutive and IFN inducible expression of MHC class II genes .
0.4985 1.0000 1.0000 Recently the MHC class II transactivator ( DNACIITA ) has been reported to be a major regulatory factor for both the constitutive and IFN inducible expression of MHC class II genes .
Recently the MHC class II transactivator ( proteinCIITA ) has been reported to be a major regulatory factor for both the constitutive and IFN inducible expression of MHC class II genes .
Recently the MHC class II transactivator ( CIITA ) has been reported to be a proteinmajor regulatory factor for both the constitutive and IFN inducible expression of MHC class II genes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2947 20.5351 10.8520 Here we show that cell_typehuman T cells expressing MHC class II have CIITA transcripts while MHC class II-negative human T cells and mouse T cells do not.
1.4116 10.6595 0.9736 Here we show that human T cells expressing MHC class II have proteinCIITA transcripts while MHC class II-negative human T cells and mouse T cells do not.
4.2466 20.9307 20.4238 Here we show that human T cells expressing MHC class II have CIITA transcripts while cell_lineMHC class II-negative human T cells and mouse T cells do not.
3.3358 20.3196 10.6207 Here we show that human T cells expressing proteinMHC class II have CIITA transcripts while MHC class II-negative human T cells and mouse T cells do not.
1.5105 10.4724 0.9996 Here we show that human T cells expressing MHC class II have RNACIITA transcripts while MHC class II-negative human T cells and mouse T cells do not.
Here we show that human T cells expressing MHC class II have CIITA transcripts while MHC class II-negative human T cells and cell_typemouse T cells do not.
Here we show that human T cells expressing MHC class II have CIITA transcripts while MHC class II-negative cell_typehuman T cells and mouse T cells do not.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.4878 20.6817 20.0030 The expression of DNAMHC class II genes in mouse T cells can be reconstituted upon transfection with the human CIITA cDNA .
3.0673 20.7108 10.0178 The expression of MHC class II genes in mouse T cells can be reconstituted upon transfection with the DNAhuman CIITA cDNA .
2.7447 10.8788 10.7374 The expression of MHC class II genes in cell_typemouse T cells can be reconstituted upon transfection with the human CIITA cDNA .
0.8746 1.0000 0.9865 The expression of MHC class II genes in mouse T cells can be reconstituted upon transfection with the human proteinCIITA cDNA .
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3.9290 20.5037 10.5235 These data indicate that the expression of CIITA explains the expression or lack of expression of proteinMHC class II in human and mouse T cells respectively.
1.5694 10.6424 1.0000 These data indicate that the expression of proteinCIITA explains the expression or lack of expression of MHC class II in human and mouse T cells respectively.
These data indicate that the expression of CIITA explains the expression or lack of expression of MHC class II in cell_typehuman and mouse T cells respectively.
These data indicate that the expression of CIITA explains the expression or lack of expression of MHC class II in human and cell_typemouse T cells respectively.
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4.5900 20.4843 10.9752 Anti-Ro(SSA) autoantibodies are associated with DNAT cell receptor beta genes in systemic lupus erythematosus patients .
0.7473 0.9943 0.9999 proteinAnti-Ro(SSA) autoantibodies are associated with T cell receptor beta genes in systemic lupus erythematosus patients .
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0.8980 1.0000 1.0000 Several of the heterogeneous clinical manifestations of systemic lupus erythematosus have been associated with specific proteinautoantibodies .
1.4987 10.8266 0.9998 Several of the heterogeneous clinical manifestations of systemic lupus erythematosus have been associated with proteinspecific autoantibodies .
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3.0178 10.8527 10.7834 Associations between proteinHLA class II antigens and autoantibodies to the ribonucleoproteins Ro(SSA) and La(SSB) have been reported in these patients.
1.4640 10.4879 1.0000 Associations between HLA class II antigens and autoantibodies to the proteinribonucleoproteins Ro(SSA) and La(SSB) have been reported in these patients.
0.9281 1.0000 1.0000 Associations between HLA class II antigens and proteinautoantibodies to the ribonucleoproteins Ro(SSA) and La(SSB) have been reported in these patients.
0.6208 0.9999 1.0000 Associations between HLA class II antigens and autoantibodies to the ribonucleoproteins proteinRo(SSA) and La(SSB) have been reported in these patients.
0.5932 1.0000 1.0000 Associations between HLA class II antigens and autoantibodies to the ribonucleoproteins Ro(SSA) and proteinLa(SSB) have been reported in these patients.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6827 30.2686 10.9883 Because HLA class II molecules present antigen to T cell receptors ( TCRs ), we have searched for a TCR gene associated with the production of proteinanti- Ro(SSA) antibodies .
3.4443 20.3555 10.4299 Because HLA class II molecules present antigen to proteinT cell receptors ( TCRs ), we have searched for a TCR gene associated with the production of anti- Ro(SSA) antibodies .
2.2791 10.9314 10.0714 Because proteinHLA class II molecules present antigen to T cell receptors ( TCRs ), we have searched for a TCR gene associated with the production of anti- Ro(SSA) antibodies .
2.0264 20.9680 1.0000 Because HLA class II molecules present antigen to T cell receptors ( TCRs ), we have searched for a DNATCR gene associated with the production of anti- Ro(SSA) antibodies .
0.9635 1.0000 1.0000 Because HLA class II molecules present antigen to T cell receptors ( proteinTCRs ), we have searched for a TCR gene associated with the production of anti- Ro(SSA) antibodies .
Because HLA class II molecules present antigen to T cell receptors ( TCRs ), we have searched for a TCR gene associated with the production of anti- proteinRo(SSA) antibodies .
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4.5279 30.0431 10.9791 A pair of restriction fragment length polymorphisms ( RFLPs ), one of which hybridizes to the TCR constant region C beta 1 and the other to the DNAC beta 2 gene , has been identified, suggesting these may be genotypic markers for an extended region of the TCR beta locus .
4.4271 30.6943 10.7708 A pair of restriction fragment length polymorphisms ( RFLPs ), one of which hybridizes to the DNATCR constant region C beta 1 and the other to the C beta 2 gene , has been identified, suggesting these may be genotypic markers for an extended region of the TCR beta locus .
4.3099 20.4742 10.9091 A pair of DNArestriction fragment length polymorphisms ( RFLPs ), one of which hybridizes to the TCR constant region C beta 1 and the other to the C beta 2 gene , has been identified, suggesting these may be genotypic markers for an extended region of the TCR beta locus .
4.0274 30.3343 10.7166 A pair of restriction fragment length polymorphisms ( RFLPs ), one of which hybridizes to the TCR constant region C beta 1 and the other to the C beta 2 gene , has been identified, suggesting these may be genotypic markers for an extended region of the DNATCR beta locus .
0.9301 1.0000 1.0000 A pair of restriction fragment length polymorphisms ( DNARFLPs ), one of which hybridizes to the TCR constant region C beta 1 and the other to the C beta 2 gene , has been identified, suggesting these may be genotypic markers for an extended region of the TCR beta locus .
1.5907 0.9863 10.9925 A pair of restriction fragment length polymorphisms ( RFLPs ), one of which hybridizes to the TCR constant region DNAC beta 1 and the other to the C beta 2 gene , has been identified, suggesting these may be genotypic markers for an extended region of the TCR beta locus .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5992 10.0279 1.0000 This DNARFLP pair occurs in 76% of patients with Ro(SSA) precipitins, 84% of anti- Ro(SSA) -positive patients lacking La(SSB) precipitins , but only 41% of the patients lacking both precipitins (P = 0.0004).
0.9073 1.0000 1.0000 This RFLP pair occurs in 76% of patients with Ro(SSA) precipitins, 84% of anti- proteinRo(SSA) -positive patients lacking La(SSB) precipitins , but only 41% of the patients lacking both precipitins (P = 0.0004).
0.8253 1.0000 1.0000 This RFLP pair occurs in 76% of patients with Ro(SSA) precipitins, 84% of anti- Ro(SSA) -positive patients lacking La(SSB) precipitins , but only 41% of the patients lacking both proteinprecipitins (P = 0.0004).
2.3109 20.0765 1.0000 This RFLP pair occurs in 76% of patients with Ro(SSA) precipitins, 84% of anti- Ro(SSA) -positive patients lacking proteinLa(SSB) precipitins , but only 41% of the patients lacking both precipitins (P = 0.0004).
This RFLP pair occurs in 76% of patients with Ro(SSA) precipitins, 84% of anti- Ro(SSA) -positive patients lacking La(SSB) proteinprecipitins , but only 41% of the patients lacking both precipitins (P = 0.0004).
This RFLP pair occurs in 76% of patients with Ro(SSA) precipitins, 84% of anti- Ro(SSA) -positive patients lacking proteinLa(SSB) precipitins , but only 41% of the patients lacking both precipitins (P = 0.0004).
This RFLP pair occurs in 76% of patients with proteinRo(SSA) precipitins, 84% of anti- Ro(SSA) -positive patients lacking La(SSB) precipitins , but only 41% of the patients lacking both precipitins (P = 0.0004).
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.2465 20.9584 10.5278 This disproportionate occurrence in a subset of lupus patients indicates that these RFLPs are not disease susceptibility markers, but rather are important markers for TCR genes whose products are involved in the production of proteinanti- Ro(SSA) antibodies .
2.3255 20.5591 1.0000 This disproportionate occurrence in a subset of lupus patients indicates that these RFLPs are not disease susceptibility markers, but rather are important markers for DNATCR genes whose products are involved in the production of anti- Ro(SSA) antibodies .
1.6786 10.3978 1.0000 This disproportionate occurrence in a subset of lupus patients indicates that these DNARFLPs are not disease susceptibility markers, but rather are important markers for TCR genes whose products are involved in the production of anti- Ro(SSA) antibodies .
This disproportionate occurrence in a subset of lupus patients indicates that these RFLPs are not disease susceptibility markers, but rather are important markers for TCR genes whose products are involved in the production of anti- proteinRo(SSA) antibodies .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0734 20.2231 10.5663 The majority of patients who have these RFLPs and proteinHLA class II antigens previously associated with the anti- Ro(SSA) response make this antibody, suggesting that interactions between products of these loci occur in response to Ro(SSA) .
1.5378 10.3635 1.0000 The majority of patients who have these DNARFLPs and HLA class II antigens previously associated with the anti- Ro(SSA) response make this antibody, suggesting that interactions between products of these loci occur in response to Ro(SSA) .
0.9295 1.0000 1.0000 The majority of patients who have these RFLPs and HLA class II antigens previously associated with the anti- proteinRo(SSA) response make this antibody, suggesting that interactions between products of these loci occur in response to Ro(SSA) .
0.8565 1.0000 1.0000 The majority of patients who have these RFLPs and HLA class II antigens previously associated with the anti- Ro(SSA) response make this antibody, suggesting that interactions between products of these loci occur in response to proteinRo(SSA) .
1.2340 10.9988 0.9999 The majority of patients who have these RFLPs and HLA class II antigens previously associated with the proteinanti- Ro(SSA) response make this antibody, suggesting that interactions between products of these loci occur in response to Ro(SSA) .
The majority of patients who have these RFLPs and HLA class II antigens previously associated with the anti- Ro(SSA) response make this antibody, suggesting that interactions between products of these DNAloci occur in response to Ro(SSA) .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8821 20.6828 10.9560 Inhibition of NF-AT -dependent transcription by NF-kappa B : implications for differential gene expression in cell_typeT helper cell subsets .
2.0363 20.1604 1.0000 Inhibition of NF-AT -dependent transcription by proteinNF-kappa B : implications for differential gene expression in T helper cell subsets .
1.4649 10.4748 1.0000 Inhibition of proteinNF-AT -dependent transcription by NF-kappa B : implications for differential gene expression in T helper cell subsets .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.9751 1.0000 1.0000 Activation of individual CD4+ T cells results in differential lymphokine expression : interleukin 2 ( proteinIL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
0.9385 1.0000 1.0000 Activation of individual CD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas proteinIL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
0.8335 1.0000 1.0000 Activation of individual CD4+ T cells results in differential proteinlymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
0.7893 1.0000 1.0000 Activation of individual CD4+ T cells results in differential lymphokine expression : proteininterleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
7.9361 30.9189 20.6497 Activation of individual CD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by cell_typeT helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
3.4118 20.5276 10.9508 Activation of individual cell_typeCD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
2.1605 20.6039 0.9999 Activation of individual CD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by cell_typeTH2 cells , which are essential for humoral immunity .
Activation of individual CD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by cell_lineTH2 cells , which are essential for humoral immunity .
Activation of individual CD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by cell_lineT helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
Activation of individual cell_lineCD4+ T cells results in differential lymphokine expression : interleukin 2 ( IL-2 ) is preferentially produced by T helper type 1 (TH1) cells , which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells , which are essential for humoral immunity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2189 10.8532 10.4255 The proteinCa(2+) -dependent factor NF-ATp plays a key role in the inducible transcription of both these lymphokine genes .
2.1306 20.4829 0.9999 The Ca(2+) -dependent factor NF-ATp plays a key role in the inducible transcription of both these DNAlymphokine genes .
0.9833 1.0000 1.0000 The Ca(2+) -dependent factor proteinNF-ATp plays a key role in the inducible transcription of both these lymphokine genes .
1.9183 20.6281 0.9810 The Ca(2+) -dependent factor NF-ATp plays a key role in the inducible transcription of both these proteinlymphokine genes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.4104 20.5225 10.9213 However, while IL2 expression requires the contribution of Ca(2+)- and proteinprotein kinase C -dependent signals , we report that activation of human IL4 transcription through the Ca(2+)-dependent pathway is diminished by protein kinase C stimulation in Jurkat T cells .
4.3556 20.6255 10.9259 However, while IL2 expression requires the contribution of Ca(2+)- and protein kinase C -dependent signals , we report that activation of human IL4 transcription through the Ca(2+)-dependent pathway is diminished by protein kinase C stimulation in cell_lineJurkat T cells .
3.6588 20.7982 10.8496 However, while IL2 expression requires the contribution of Ca(2+)- and protein kinase C -dependent signals , we report that activation of human IL4 transcription through the Ca(2+)-dependent pathway is diminished by proteinprotein kinase C stimulation in Jurkat T cells .
0.9022 1.0000 1.0000 However, while proteinIL2 expression requires the contribution of Ca(2+)- and protein kinase C -dependent signals , we report that activation of human IL4 transcription through the Ca(2+)-dependent pathway is diminished by protein kinase C stimulation in Jurkat T cells .
0.9196 0.9999 1.0000 However, while IL2 expression requires the contribution of Ca(2+)- and protein kinase C -dependent signals , we report that activation of human proteinIL4 transcription through the Ca(2+)-dependent pathway is diminished by protein kinase C stimulation in Jurkat T cells .
However, while IL2 expression requires the contribution of Ca(2+)- and protein kinase C -dependent signals , we report that activation of proteinhuman IL4 transcription through the Ca(2+)-dependent pathway is diminished by protein kinase C stimulation in Jurkat T cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8098 20.5230 10.8664 This phenomenon is due to mutually exclusive binding of NF-ATp and NF-kappa B to the P sequence , an element located 69 bp upstream of the DNAIL4 transcription initiation site .
3.6195 20.4897 10.8147 This phenomenon is due to mutually exclusive binding of NF-ATp and NF-kappa B to the P sequence , an element located DNA69 bp upstream of the IL4 transcription initiation site .
1.6003 10.3813 1.0000 This phenomenon is due to mutually exclusive binding of proteinNF-ATp and NF-kappa B to the P sequence , an element located 69 bp upstream of the IL4 transcription initiation site .
1.5877 10.1762 1.0000 This phenomenon is due to mutually exclusive binding of NF-ATp and proteinNF-kappa B to the P sequence , an element located 69 bp upstream of the IL4 transcription initiation site .
1.4116 10.9174 1.0000 This phenomenon is due to mutually exclusive binding of NF-ATp and NF-kappa B to the DNAP sequence , an element located 69 bp upstream of the IL4 transcription initiation site .
2.0454 20.0711 0.9981 This phenomenon is due to mutually exclusive binding of NF-ATp and NF-kappa B to the P sequence , an element located 69 bp upstream of the proteinIL4 transcription initiation site .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.5054 20.7381 10.8209 Human IL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the proteinNF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
2.5975 20.7972 10.9009 Human IL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in cell_lineRelA -overexpressing cells .
2.0347 20.1456 0.9955 Human IL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in proteinRelA -overexpressing cells .
1.9431 20.4999 0.9151 Human IL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the proteinNF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
1.3254 0.8660 10.7058 Human IL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B -activating cytokine proteintumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
1.3004 10.8304 0.9999 Human IL4 promoter -mediated transcription is downregulated in cell_lineJurkat cells stimulated with the NF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
1.4876 10.4393 0.9999 Human DNAIL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
1.0448 10.3974 0.9751 Human proteinIL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
DNAHuman IL4 promoter -mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B -activating cytokine tumor necrosis factor alpha and suppressed in RelA -overexpressing cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.2151 20.5296 10.8455 In contrast, proteinprotein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
3.5735 20.9514 10.7503 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a DNAhuman IL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
3.5429 20.6922 10.5856 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a DNAmouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
2.0892 20.1007 0.9994 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a DNAlower-affinity site for RelA .
2.0402 20.6748 0.9993 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence , which is a DNAhigher-affinity site for NF-ATp and a lower-affinity site for RelA .
1.6079 10.1009 1.0000 In contrast, protein kinase C stimulation or proteinRelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
0.9068 0.9999 1.0000 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence , which is a higher-affinity site for proteinNF-ATp and a lower-affinity site for RelA .
0.8071 0.9999 1.0000 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for proteinRelA .
0.6391 0.9999 0.9997 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse DNAP sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
0.7274 0.9997 0.9997 In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human DNAIL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a proteinhuman IL4 promoter containing a mouse P sequence , which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.6836 20.9225 10.8346 Thus, competition between two general transcriptional activators , RelA and NF-ATp , mediates the inhibitory effect of proteinprotein kinase C stimulation on IL4 expression and may contribute to differential gene expression in TH cells .
1.7179 10.5049 1.0000 Thus, competition between two general transcriptional activators , proteinRelA and NF-ATp , mediates the inhibitory effect of protein kinase C stimulation on IL4 expression and may contribute to differential gene expression in TH cells .
1.6117 10.5188 1.0000 Thus, competition between two general transcriptional activators , RelA and NF-ATp , mediates the inhibitory effect of protein kinase C stimulation on proteinIL4 expression and may contribute to differential gene expression in TH cells .
1.3751 10.4281 1.0000 Thus, competition between two general proteintranscriptional activators , RelA and NF-ATp , mediates the inhibitory effect of protein kinase C stimulation on IL4 expression and may contribute to differential gene expression in TH cells .
0.8899 1.0000 1.0000 Thus, competition between two general transcriptional activators , RelA and proteinNF-ATp , mediates the inhibitory effect of protein kinase C stimulation on IL4 expression and may contribute to differential gene expression in TH cells .
2.2781 20.9623 0.9999 Thus, competition between two general transcriptional activators , RelA and NF-ATp , mediates the inhibitory effect of protein kinase C stimulation on IL4 expression and may contribute to differential gene expression in cell_typeTH cells .
Thus, competition between two general transcriptional activators , RelA and NF-ATp , mediates the inhibitory effect of protein kinase C stimulation on IL4 expression and may contribute to differential gene expression in cell_lineTH cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.3430 10.3024 1.0000 Regulation of the balance of proteincytokine production and the signal transducer and activator of transcription ( STAT ) transcription factor activity by cytokines and inflammatory synovial fluids.
0.8292 0.9998 1.0000 Regulation of the balance of cytokine production and the signal transducer and activator of transcription ( STAT ) transcription factor activity by proteincytokines and inflammatory synovial fluids.
5.7182 10.5864 30.8088 Regulation of the balance of cytokine production and the proteinsignal transducer and activator of transcription ( STAT ) transcription factor activity by cytokines and inflammatory synovial fluids.
Regulation of the balance of cytokine production and the signal transducer and activator of transcription ( proteinSTAT ) transcription factor activity by cytokines and inflammatory synovial fluids.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8118 10.0782 1.0000 The balance between type 1 and 2 T helper cell cytokine production plays an important role in several animal models of autoimmunity, and skewed patterns of proteincytokine expression have been described in human inflammatory diseases .
0.9552 0.9999 1.0000 The balance between type 1 and 2 T helper cell proteincytokine production plays an important role in several animal models of autoimmunity, and skewed patterns of cytokine expression have been described in human inflammatory diseases .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.9802 10.6994 30.0640 Many cytokines activate proteinsignal transducer and activation of transcription ( STAT ) transcription factors , which, in turn, activate transcription of inflammatory effector genes.
0.6895 0.9922 0.9998 Many proteincytokines activate signal transducer and activation of transcription ( STAT ) transcription factors , which, in turn, activate transcription of inflammatory effector genes.
Many cytokines activate signal transducer and activation of transcription ( proteinSTAT ) transcription factors , which, in turn, activate transcription of inflammatory effector genes.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.6809 20.7793 10.9182 We used cell_linemononuclear cell priming cultures and inflammatory synovial fluids ( SFs ) derived from arthritis patients to examine the regulation of cytokine production and STAT activity by an inflammatory synovial microenvironment .
1.6529 10.6761 1.0000 We used mononuclear cell priming cultures and inflammatory synovial fluids ( SFs ) derived from arthritis patients to examine the regulation of cytokine production and proteinSTAT activity by an inflammatory synovial microenvironment .
0.8988 0.9999 1.0000 We used mononuclear cell priming cultures and inflammatory synovial fluids ( SFs ) derived from arthritis patients to examine the regulation of proteincytokine production and STAT activity by an inflammatory synovial microenvironment .
We used mononuclear cell priming cultures and inflammatory synovial fluids ( cell_typeSFs ) derived from arthritis patients to examine the regulation of cytokine production and STAT activity by an inflammatory synovial microenvironment .
We used mononuclear cell priming cultures and cell_typeinflammatory synovial fluids ( SFs ) derived from arthritis patients to examine the regulation of cytokine production and STAT activity by an inflammatory synovial microenvironment .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2059 20.3432 1.0000 Exposure to SFs during priming resulted in an 81% inhibition of proteininterferon (IFN)-gamma , but not interleukin (IL) 4 , production by effector cells generated in priming cultures.
2.1914 20.0890 0.9999 Exposure to SFs during priming resulted in an 81% inhibition of interferon (IFN)-gamma , but not proteininterleukin (IL) 4 , production by effector cells generated in priming cultures.
1.4484 10.8317 0.9999 Exposure to SFs during priming resulted in an 81% inhibition of interferon (IFN)-gamma , but not interleukin (IL) 4 , production by cell_typeeffector cells generated in priming cultures.
1.5726 20.2025 0.7286 Exposure to SFs during priming resulted in an 81% inhibition of interferon (IFN)-gamma , but not proteininterleukin (IL) 4 , production by effector cells generated in priming cultures.
Exposure to cell_typeSFs during priming resulted in an 81% inhibition of interferon (IFN)-gamma , but not interleukin (IL) 4 , production by effector cells generated in priming cultures.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7401 10.1365 1.0000 SF suppression was mediated by proteinIL-4 and IL-10 and inhibition of IL-12 expression , and it was reversed in a dominant fashion by exogenous IL-12.
1.6381 10.8163 1.0000 SF suppression was mediated by IL-4 and IL-10 and inhibition of proteinIL-12 expression , and it was reversed in a dominant fashion by exogenous IL-12.
0.9668 1.0000 1.0000 SF suppression was mediated by IL-4 and proteinIL-10 and inhibition of IL-12 expression , and it was reversed in a dominant fashion by exogenous IL-12.
0.6487 1.0000 1.0000 proteinSF suppression was mediated by IL-4 and IL-10 and inhibition of IL-12 expression , and it was reversed in a dominant fashion by exogenous IL-12.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7921 10.0029 1.0000 SFs blocked the sustained activity of transcription factor Stat1 , but not proteinStat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
1.7220 10.3273 1.0000 SFs blocked the sustained activity of transcription factor Stat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by proteincytokines in parallel with their positive or negative regulation of IFN-gamma production .
1.6349 10.8251 1.0000 SFs blocked the sustained activity of transcription factor Stat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of proteinIFN-gamma production .
0.9500 1.0000 1.0000 SFs blocked the sustained activity of transcription factor Stat1 , but not Stat3 , during the priming period, and proteinStat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
2.2615 20.5572 0.9998 SFs blocked the sustained activity of proteintranscription factor Stat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
0.9794 1.0000 1.0000 proteinSFs blocked the sustained activity of transcription factor Stat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
0.9697 1.0000 1.0000 SFs blocked the sustained activity of transcription factor proteinStat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
cell_typeSFs blocked the sustained activity of transcription factor Stat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
SFs blocked the sustained activity of proteintranscription factor Stat1 , but not Stat3 , during the priming period, and Stat1 activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-gamma production .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5861 10.6609 1.0000 Active Stat3 , but not proteinStat1 , was detected in cells from inflamed joints .
0.8956 0.9999 1.0000 Active proteinStat3 , but not Stat1 , was detected in cells from inflamed joints .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6522 10.3509 0.9999 These results suggest a role for altered balance of Stat1 and Stat3 transcriptional activity in the regulation of cell_typeT cell differentiation and in the pathogenesis of inflammatory synovitis .
1.7176 10.4051 1.0000 These results suggest a role for altered balance of proteinStat1 and Stat3 transcriptional activity in the regulation of T cell differentiation and in the pathogenesis of inflammatory synovitis .
0.9154 0.9999 1.0000 These results suggest a role for altered balance of Stat1 and proteinStat3 transcriptional activity in the regulation of T cell differentiation and in the pathogenesis of inflammatory synovitis .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.4251 30.2852 10.1770 Triggering of complement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in cell_typeHIV-infected monocytic cells .
2.0980 20.3745 1.0000 Triggering of complement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of proteinNF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
1.8236 10.3005 1.0000 Triggering of complement receptors CR1 ( CD35 ) and proteinCR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
1.3719 10.7345 0.9999 Triggering of complement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in cell_typehuman monocytes and enhances viral replication in HIV-infected monocytic cells .
1.3277 20.8590 0.9993 Triggering of proteincomplement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
0.9763 1.0000 1.0000 Triggering of complement receptors CR1 ( proteinCD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
0.9579 1.0000 1.0000 Triggering of complement receptors proteinCR1 ( CD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
0.9370 1.0000 1.0000 Triggering of complement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) induces nuclear translocation of NF-kappa B ( proteinp50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
0.9341 1.0000 1.0000 Triggering of complement receptors CR1 ( CD35 ) and CR3 ( proteinCD11b/CD18 ) induces nuclear translocation of NF-kappa B ( p50/p65 ) in human monocytes and enhances viral replication in HIV-infected monocytic cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
0.8829 1.0000 1.0000 cell_typeMonocyte/macrophages may harbor HIV in a nonproductive fashion for prolonged periods of time.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7429 10.2713 1.0000 Viral gene expression may be reactivated by stimulation of the cells with LPS or proteincytokines such as TNF-alpha in vitro.
1.6615 10.7407 1.0000 Viral gene expression may be reactivated by stimulation of the cells with LPS or cytokines such as proteinTNF-alpha in vitro.
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.5329 30.0273 10.5606 The effect of LPS and TNF-alpha is mediated by their ability to induce nuclear translocation of the DNA-binding heterodimer NF-kappa B ( p50/p65 ), which binds to a specific sequence in the DNAHIV-long terminal repeat .
2.1519 20.1517 0.9997 The effect of LPS and TNF-alpha is mediated by their ability to induce nuclear translocation of the proteinDNA-binding heterodimer NF-kappa B ( p50/p65 ), which binds to a specific sequence in the HIV-long terminal repeat .
1.6769 10.3817 1.0000 The effect of LPS and proteinTNF-alpha is mediated by their ability to induce nuclear translocation of the DNA-binding heterodimer NF-kappa B ( p50/p65 ), which binds to a specific sequence in the HIV-long terminal repeat .
0.9780 1.0000 1.0000 The effect of LPS and TNF-alpha is mediated by their ability to induce nuclear translocation of the DNA-binding heterodimer NF-kappa B ( proteinp50/p65 ), which binds to a specific sequence in the HIV-long terminal repeat .
0.9047 0.9998 0.9999 The effect of LPS and TNF-alpha is mediated by their ability to induce nuclear translocation of the DNA-binding heterodimer proteinNF-kappa B ( p50/p65 ), which binds to a specific sequence in the HIV-long terminal repeat .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.8577 20.8337 0.9996 The present study demonstrates that triggering of proteincomplement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) enhances viral replication in HIV-infected human monocytic cells .
1.6929 10.3883 1.0000 The present study demonstrates that triggering of complement receptors CR1 ( CD35 ) and proteinCR3 ( CD11b/CD18 ) enhances viral replication in HIV-infected human monocytic cells .
0.9572 1.0000 1.0000 The present study demonstrates that triggering of complement receptors CR1 ( proteinCD35 ) and CR3 ( CD11b/CD18 ) enhances viral replication in HIV-infected human monocytic cells .
0.9491 1.0000 1.0000 The present study demonstrates that triggering of complement receptors proteinCR1 ( CD35 ) and CR3 ( CD11b/CD18 ) enhances viral replication in HIV-infected human monocytic cells .
0.9180 1.0000 1.0000 The present study demonstrates that triggering of complement receptors CR1 ( CD35 ) and CR3 ( proteinCD11b/CD18 ) enhances viral replication in HIV-infected human monocytic cells .
4.6792 20.9611 10.6090 The present study demonstrates that triggering of complement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) enhances viral replication in cell_typeHIV-infected human monocytic cells .
The present study demonstrates that triggering of complement receptors CR1 ( CD35 ) and CR3 ( CD11b/CD18 ) enhances viral replication in cell_lineHIV-infected human monocytic cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.9869 10.6108 10.7354 Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of proteinmonoclonal anti- CR1 or anti- CR3 Abs or with C3 fragments .
2.2680 10.6580 10.2266 Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti- CR1 or proteinanti- CR3 Abs or with C3 fragments .
2.1120 20.7275 0.9998 Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of proteinF(ab')2 fragments of monoclonal anti- CR1 or anti- CR3 Abs or with C3 fragments .
1.4823 0.9955 10.0407 cell_lineMonocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti- CR1 or anti- CR3 Abs or with C3 fragments .
1.3026 10.6378 0.9996 Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti- CR1 or anti- CR3 Abs or with proteinC3 fragments .
0.8851 1.0000 0.9821 Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti- CR1 or anti- proteinCR3 Abs or with C3 fragments .
0.8820 1.0000 1.0000 Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti- proteinCR1 or anti- CR3 Abs or with C3 fragments .
3.9778 20.8725 10.8612 Monocytic cell lines and cell_typenormal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti- CR1 or anti- CR3 Abs or with C3 fragments .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3862 20.0552 1.0000 Stimulation of CR1 or CR3 induces a two- to fourfold increase in the amount of cell-associated and released proteinp24 Ag in cell cultures that was equivalent to that observed in control cultures triggered with LPS .
1.6316 10.9877 1.0000 Stimulation of proteinCR1 or CR3 induces a two- to fourfold increase in the amount of cell-associated and released p24 Ag in cell cultures that was equivalent to that observed in control cultures triggered with LPS .
1.5684 10.2887 0.9993 Stimulation of CR1 or CR3 induces a two- to fourfold increase in the amount of cell-associated and released p24 Ag in cell_linecell cultures that was equivalent to that observed in control cultures triggered with LPS .
1.3702 10.6644 0.9999 Stimulation of CR1 or CR3 induces a two- to fourfold increase in the amount of cell-associated and released p24 Ag in cell cultures that was equivalent to that observed in cell_linecontrol cultures triggered with LPS .
0.8925 1.0000 1.0000 Stimulation of CR1 or proteinCR3 induces a two- to fourfold increase in the amount of cell-associated and released p24 Ag in cell cultures that was equivalent to that observed in control cultures triggered with LPS .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1325 20.9483 0.9958 We further observed that stimulation of CR1 or CR3 induces the nuclear translocation of proteinNF-kappa B p50/p65 in infected cells .
1.5641 10.1639 0.9996 We further observed that stimulation of CR1 or CR3 induces the nuclear translocation of NF-kappa B p50/p65 in cell_typeinfected cells .
1.4320 10.8612 1.0000 We further observed that stimulation of proteinCR1 or CR3 induces the nuclear translocation of NF-kappa B p50/p65 in infected cells .
0.9816 1.0000 1.0000 We further observed that stimulation of CR1 or CR3 induces the nuclear translocation of NF-kappa B proteinp50/p65 in infected cells .
0.8442 0.9999 1.0000 We further observed that stimulation of CR1 or proteinCR3 induces the nuclear translocation of NF-kappa B p50/p65 in infected cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.8423 20.9127 10.5641 Translocation of NF-kappa B p50/p65 was also observed following stimulation of CR1 or CR3 of cell_typeuninfected peripheral blood monocytes from HIV-seronegative donors .
1.4284 10.6371 1.0000 Translocation of NF-kappa B p50/p65 was also observed following stimulation of proteinCR1 or CR3 of uninfected peripheral blood monocytes from HIV-seronegative donors .
0.8039 0.9986 1.0000 Translocation of NF-kappa B p50/p65 was also observed following stimulation of CR1 or proteinCR3 of uninfected peripheral blood monocytes from HIV-seronegative donors .
2.2040 20.9972 10.5615 Translocation of proteinNF-kappa B p50/p65 was also observed following stimulation of CR1 or CR3 of uninfected peripheral blood monocytes from HIV-seronegative donors .
Translocation of NF-kappa B proteinp50/p65 was also observed following stimulation of CR1 or CR3 of uninfected peripheral blood monocytes from HIV-seronegative donors .
Translocation of proteinNF-kappa B p50/p65 was also observed following stimulation of CR1 or CR3 of uninfected peripheral blood monocytes from HIV-seronegative donors .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6061 10.9362 1.0000 The amount of protein translocated was similar to that observed when cells were stimulated with proteinrhTNF-alpha .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.9934 20.4313 0.9999 TNF-alpha did not mediate the translocation of NF-kappa B p50/p65 induced by triggering of proteincomplement receptors .
1.7188 20.8611 0.8683 TNF-alpha did not mediate the translocation of proteinNF-kappa B p50/p65 induced by triggering of complement receptors .
0.9623 1.0000 1.0000 proteinTNF-alpha did not mediate the translocation of NF-kappa B p50/p65 induced by triggering of complement receptors .
2.2943 20.8430 1.0000 TNF-alpha did not mediate the translocation of proteinNF-kappa B p50/p65 induced by triggering of complement receptors .
TNF-alpha did not mediate the translocation of NF-kappa B proteinp50/p65 induced by triggering of complement receptors .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2683 20.5202 0.9999 Taken together, these observations suggest that HIV gene expression may be activated in cell_typeinfected monocytes through interaction of the cells with complement-opsonized particles and that enhanced viral replication is associated with C3 receptor -mediated nuclear translocation of the NF-kappa B complex .
2.2297 20.9123 0.9999 Taken together, these observations suggest that HIV gene expression may be activated in infected monocytes through interaction of the cells with complement-opsonized particles and that enhanced viral replication is associated with C3 receptor -mediated nuclear translocation of the proteinNF-kappa B complex .
1.5830 10.9952 1.0000 Taken together, these observations suggest that HIV gene expression may be activated in infected monocytes through interaction of the cells with complement-opsonized particles and that enhanced viral replication is associated with proteinC3 receptor -mediated nuclear translocation of the NF-kappa B complex .
2.8190 30.0654 0.8758 Taken together, these observations suggest that HIV gene expression may be activated in infected monocytes through interaction of the cells with complement-opsonized particles and that enhanced viral replication is associated with C3 receptor -mediated nuclear translocation of the proteinNF-kappa B complex .
0.8784 1.0000 1.0000 Taken together, these observations suggest that HIV gene expression may be activated in infected cell_typemonocytes through interaction of the cells with complement-opsonized particles and that enhanced viral replication is associated with C3 receptor -mediated nuclear translocation of the NF-kappa B complex .
Taken together, these observations suggest that HIV gene expression may be activated in infected monocytes through interaction of the cells with proteincomplement-opsonized particles and that enhanced viral replication is associated with C3 receptor -mediated nuclear translocation of the NF-kappa B complex .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2998 20.2391 1.0000 Attenuation of gamma interferon -induced tyrosine phosphorylation in cell_typemononuclear phagocytes infected with Leishmania donovani : selective inhibition of signaling through Janus kinases and Stat1 .
2.2495 20.3747 1.0000 Attenuation of proteingamma interferon -induced tyrosine phosphorylation in mononuclear phagocytes infected with Leishmania donovani : selective inhibition of signaling through Janus kinases and Stat1 .
2.2018 20.9291 1.0000 Attenuation of gamma interferon -induced tyrosine phosphorylation in mononuclear phagocytes infected with Leishmania donovani : selective inhibition of signaling through proteinJanus kinases and Stat1 .
1.6571 10.3795 1.0000 Attenuation of gamma interferon -induced tyrosine phosphorylation in mononuclear phagocytes infected with Leishmania donovani : selective inhibition of signaling through Janus kinases and proteinStat1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4792 20.0638 1.0000 The induction of gene transcription in response to gamma interferon is impaired in cell_typemononuclear phagocytes infected with Leishmania donovani , and the mechanisms involved are not fully understood.
2.4505 20.4933 1.0000 The induction of gene transcription in response to proteingamma interferon is impaired in mononuclear phagocytes infected with Leishmania donovani , and the mechanisms involved are not fully understood.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9825 20.7808 10.7568 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of proteincellular protein tyrosine kinases , including the Janus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the transcription factor Stat1 .
2.1275 20.5035 0.9998 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the proteinJanus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the transcription factor Stat1 .
1.4639 10.9722 1.0000 The changes in gene expression brought about by proteingamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the Janus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the transcription factor Stat1 .
0.9631 1.0000 1.0000 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the Janus kinases Jak1 and proteinJak2 , leading to tyrosine phosphorylation of the transcription factor Stat1 .
0.9585 1.0000 1.0000 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the Janus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the transcription factor proteinStat1 .
0.9517 1.0000 1.0000 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the Janus kinases proteinJak1 and Jak2 , leading to tyrosine phosphorylation of the transcription factor Stat1 .
2.1092 20.9650 0.9995 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the Janus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the proteintranscription factor Stat1 .
0.6846 0.9982 0.9999 The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein proteintyrosine kinases , including the Janus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the transcription factor Stat1 .
The changes in gene expression brought about by gamma interferon are thought to involve transient increases in the activities of cellular protein tyrosine kinases , including the Janus kinases Jak1 and Jak2 , leading to tyrosine phosphorylation of the proteintranscription factor Stat1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
7.4754 30.3772 20.7922 To investigate the mechanisms accounting for the impaired responses to gamma interferon , a model system for examining overall changes in protein tyrosine phosphorylation , activation of Jak1 and Jak2 and phosphorylation of Stat1 was developed in cell_linephorbol 12-myristate 13-acetate -differentiated U-937 cells .
2.0965 20.2732 1.0000 To investigate the mechanisms accounting for the impaired responses to gamma interferon , a model system for examining overall changes in protein tyrosine phosphorylation , activation of Jak1 and Jak2 and phosphorylation of proteinStat1 was developed in phorbol 12-myristate 13-acetate -differentiated U-937 cells .
2.0949 20.5571 1.0000 To investigate the mechanisms accounting for the impaired responses to proteingamma interferon , a model system for examining overall changes in protein tyrosine phosphorylation , activation of Jak1 and Jak2 and phosphorylation of Stat1 was developed in phorbol 12-myristate 13-acetate -differentiated U-937 cells .
1.5216 10.4264 1.0000 To investigate the mechanisms accounting for the impaired responses to gamma interferon , a model system for examining overall changes in protein tyrosine phosphorylation , activation of proteinJak1 and Jak2 and phosphorylation of Stat1 was developed in phorbol 12-myristate 13-acetate -differentiated U-937 cells .
0.9132 1.0000 1.0000 To investigate the mechanisms accounting for the impaired responses to gamma interferon , a model system for examining overall changes in protein tyrosine phosphorylation , activation of Jak1 and proteinJak2 and phosphorylation of Stat1 was developed in phorbol 12-myristate 13-acetate -differentiated U-937 cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3437 20.0782 1.0000 Analysis of whole-cell lysates by antiphosphotyrosine immunoblotting showed that incubation with proteingamma interferon brought about specific increases in phosphotyrosine labeling of several proteins.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6827 10.8227 0.9999 Increased labeling of these proteins occurred to similar extents in cell_typecontrol cells and in cells that had been infected with L. donovani for 16 h.
1.7519 10.4563 1.0000 Increased labeling of these proteinproteins occurred to similar extents in control cells and in cells that had been infected with L. donovani for 16 h.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.7479 10.3100 1.0000 Jak1 , Jak2 , and proteinStat1 were immunoprecipitated from control and interferon-treated cells , and tyrosine phosphorylation of these proteins, detected by antiphosphotyrosine immunoblotting was used to measured their activation.
1.5298 10.6802 0.9997 Jak1 , Jak2 , and Stat1 were immunoprecipitated from control and cell_lineinterferon-treated cells , and tyrosine phosphorylation of these proteins, detected by antiphosphotyrosine immunoblotting was used to measured their activation.
0.9813 1.0000 1.0000 Jak1 , proteinJak2 , and Stat1 were immunoprecipitated from control and interferon-treated cells , and tyrosine phosphorylation of these proteins, detected by antiphosphotyrosine immunoblotting was used to measured their activation.
0.9762 1.0000 1.0000 proteinJak1 , Jak2 , and Stat1 were immunoprecipitated from control and interferon-treated cells , and tyrosine phosphorylation of these proteins, detected by antiphosphotyrosine immunoblotting was used to measured their activation.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2487 20.2048 0.9999 Tyrosine phosphorylation of Jak1 , Jak2 , and Stat1 increased markedly, in a dose-dependent manner, in cell_lineU-937 cells incubated with gamma interferon .
1.6188 10.8936 1.0000 Tyrosine phosphorylation of Jak1 , Jak2 , and proteinStat1 increased markedly, in a dose-dependent manner, in U-937 cells incubated with gamma interferon .
1.5213 10.9110 1.0000 Tyrosine phosphorylation of proteinJak1 , Jak2 , and Stat1 increased markedly, in a dose-dependent manner, in U-937 cells incubated with gamma interferon .
1.4327 10.7843 0.9999 Tyrosine phosphorylation of Jak1 , Jak2 , and Stat1 increased markedly, in a dose-dependent manner, in U-937 cells incubated with proteingamma interferon .
0.9204 1.0000 1.0000 Tyrosine phosphorylation of Jak1 , proteinJak2 , and Stat1 increased markedly, in a dose-dependent manner, in U-937 cells incubated with gamma interferon .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6838 10.9321 1.0000 In contrast, in cells infected with L. donovani , tyrosine phosphorylation of Jak1 , Jak2 , and proteinStat1 was markedly impaired.
1.6355 10.7269 1.0000 In contrast, in cells infected with L. donovani , tyrosine phosphorylation of proteinJak1 , Jak2 , and Stat1 was markedly impaired.
0.9398 1.0000 1.0000 In contrast, in cells infected with L. donovani , tyrosine phosphorylation of Jak1 , proteinJak2 , and Stat1 was markedly impaired.
Cls_Score Left_Reg_Score Right_Reg_Score Text
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7771 20.9882 10.8538 Results similar to those observed with U-937 cells were also obtained with cell_typehuman peripheral blood monocytes .
2.1042 20.5117 0.9999 Results similar to those observed with cell_lineU-937 cells were also obtained with human peripheral blood monocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7056 20.7356 10.7229 These findings indicate that infection of cell_typehuman mononuclear phagocytes with L. donovani leads to impaired gamma interferon -mediated tyrosine phosphorylation and selective effects on the Jak- Stat1 pathway .
1.4880 10.5301 1.0000 These findings indicate that infection of human mononuclear phagocytes with L. donovani leads to impaired proteingamma interferon -mediated tyrosine phosphorylation and selective effects on the Jak- Stat1 pathway .
0.9714 1.0000 1.0000 These findings indicate that infection of human mononuclear phagocytes with L. donovani leads to impaired gamma interferon -mediated tyrosine phosphorylation and selective effects on the Jak- proteinStat1 pathway .
1.3243 10.8320 0.9996 These findings indicate that infection of human mononuclear phagocytes with L. donovani leads to impaired gamma interferon -mediated tyrosine phosphorylation and selective effects on the proteinJak- Stat1 pathway .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1568 20.3286 0.9999 Unresponsiveness to gamma interferon for activation of this pathway may explain impaired transcriptional responses in cell_typeleishmania-infected cells .
2.1271 20.1407 1.0000 Unresponsiveness to proteingamma interferon for activation of this pathway may explain impaired transcriptional responses in leishmania-infected cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.9999 20.7304 20.6266 Mutually exclusive interaction of a novel proteinmatrix attachment region binding protein and the NF-muNR enhancer repressor .
3.9537 30.5578 10.7874 Mutually exclusive interaction of a novel matrix attachment region binding protein and the proteinNF-muNR enhancer repressor .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.7614 10.5784 10.9647 Implications for regulation of proteinimmunoglobulin heavy chain expression .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.2948 0.9978 10.1681 The proteinimmunoglobulin heavy chain ( IgH ) intronic enhancer stimulates transcription from functional promoters in B lymphocytes but not other cell types.
0.9403 1.0000 0.9944 The immunoglobulin heavy chain ( proteinIgH ) intronic enhancer stimulates transcription from functional promoters in B lymphocytes but not other cell types.
5.0649 10.9563 20.8118 The DNAimmunoglobulin heavy chain ( IgH ) intronic enhancer stimulates transcription from functional promoters in B lymphocytes but not other cell types.
1.1722 10.5166 0.9996 The immunoglobulin heavy chain ( IgH ) intronic enhancer stimulates transcription from functional promoters in cell_typeB lymphocytes but not other cell types.
1.1210 10.9718 0.9998 The immunoglobulin heavy chain ( IgH ) intronic enhancer stimulates transcription from DNAfunctional promoters in B lymphocytes but not other cell types.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4201 10.2577 0.9999 The observation that binding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the DNAenhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
0.9576 1.0000 0.9916 The observation that binding sites for the nuclear factor-mu negative regulator ( proteinNF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
0.6248 1.0000 0.9999 The observation that binding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this DNAenhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
2.4567 20.1490 10.6710 The observation that binding sites for the proteinnuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
2.3625 10.2190 10.2173 The observation that binding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap DNAnuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
1.8335 20.6974 0.9990 The observation that DNAbinding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
0.9588 1.0000 1.0000 The observation that binding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( DNAMARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
The observation that binding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap proteinnuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
The observation that binding sites for the proteinnuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
The observation that binding sites for the proteinnuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( MARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
The observation that binding sites for the nuclear factor-mu negative regulator ( NF-muNR ) enhancer repressor overlap nuclear matrix attachment regions ( proteinMARs ) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R. H., and Chen, U. (1989) Genes & Dev. 3, 1255-1266).
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4278 20.6634 1.0000 To understand the role of MARs in IgH enhancer regulation , we have identified a novel proteinMAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer .
2.2852 20.5649 0.9999 To understand the role of MARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the DNAIgH enhancer .
0.9579 1.0000 1.0000 To understand the role of MARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , proteinMAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer .
0.7919 0.9992 0.9999 To understand the role of MARs in DNAIgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer .
1.7260 10.3638 1.0000 To understand the role of MARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the DNAMARs associated with the IgH enhancer .
1.6438 10.5533 1.0000 To understand the role of DNAMARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer .
To understand the role of MARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the proteinIgH enhancer .
To understand the role of MARs in proteinIgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer .
To understand the role of proteinMARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer .
To understand the role of MARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the proteinMARs associated with the IgH enhancer .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.7970 20.4047 10.5965 Purified MAR-BP1 migrates as a 33-kDa protein , and it can be found in nuclear matrix preparations from a number of different types of cell_linelymphoid cell lines .
2.2437 20.0575 1.0000 Purified MAR-BP1 migrates as a protein33-kDa protein , and it can be found in nuclear matrix preparations from a number of different types of lymphoid cell lines .
0.9843 1.0000 1.0000 Purified proteinMAR-BP1 migrates as a 33-kDa protein , and it can be found in nuclear matrix preparations from a number of different types of lymphoid cell lines .
0.7255 0.9981 1.0000 proteinPurified MAR-BP1 migrates as a 33-kDa protein , and it can be found in nuclear matrix preparations from a number of different types of lymphoid cell lines .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6463 10.2015 1.0000 Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures , NF-muNR binding sites are critical for efficient proteinMAR-BP1 binding .
1.3964 10.7581 0.9964 Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures , proteinNF-muNR binding sites are critical for efficient MAR-BP1 binding .
3.1595 20.8103 10.6702 Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures , DNANF-muNR binding sites are critical for efficient MAR-BP1 binding .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3105 20.4715 1.0000 Indeed, binding of the DNAIgH enhancer to either intact nuclear matrix preparations or to MAR-BP1 is mutually exclusive to NF-muNR binding .
1.6324 10.5368 1.0000 Indeed, binding of the IgH enhancer to either intact nuclear matrix preparations or to proteinMAR-BP1 is mutually exclusive to NF-muNR binding .
0.9098 1.0000 1.0000 Indeed, binding of the IgH enhancer to either intact nuclear matrix preparations or to MAR-BP1 is mutually exclusive to proteinNF-muNR binding .
Indeed, binding of the proteinIgH enhancer to either intact nuclear matrix preparations or to MAR-BP1 is mutually exclusive to NF-muNR binding .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.3125 20.2916 1.0000 These results are consistent with a model for cell-type specific regulation in which binding of the proteinNF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1 /enhancer interaction .
2.2775 20.5983 0.9931 These results are consistent with a model for cell-type specific regulation in which binding of the proteinNF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1 /enhancer interaction .
1.6438 10.0747 0.9999 These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with proteinMAR-BP1 /enhancer interaction .
1.5387 10.9752 1.0000 These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the DNAIgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1 /enhancer interaction .
0.4792 1.0000 0.9996 These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1 DNA/enhancer interaction .
1.6245 10.6559 0.9999 These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in cell_typeinappropriate cells by interfering with MAR-BP1 /enhancer interaction .
These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the proteinIgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1 /enhancer interaction .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.7639 30.6715 10.3658 PU.1 ( Spi-1 ) and C/EBP alpha regulate expression of the DNAgranulocyte-macrophage colony-stimulating factor receptor alpha gene .
1.1533 10.5214 1.0000 PU.1 ( Spi-1 ) and proteinC/EBP alpha regulate expression of the granulocyte-macrophage colony-stimulating factor receptor alpha gene .
0.9621 1.0000 1.0000 PU.1 ( proteinSpi-1 ) and C/EBP alpha regulate expression of the granulocyte-macrophage colony-stimulating factor receptor alpha gene .
0.9477 1.0000 1.0000 proteinPU.1 ( Spi-1 ) and C/EBP alpha regulate expression of the granulocyte-macrophage colony-stimulating factor receptor alpha gene .
2.4398 20.9571 10.3997 PU.1 ( Spi-1 ) and C/EBP alpha regulate expression of the proteingranulocyte-macrophage colony-stimulating factor receptor alpha gene .
PU.1 ( Spi-1 ) and C/EBP alpha regulate expression of the proteingranulocyte-macrophage colony-stimulating factor receptor alpha gene .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6167 0.9985 10.6846 proteinGrowth factor receptors play an important role in hematopoiesis .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.4912 40.7452 10.0588 In order to further understand the mechanisms directing the expression of these key regulators of hematopoiesis , we initiated a study investigating the transcription factors activating the expression of the proteingranulocyte-macrophage colony-stimulating factor ( GM-CSF ) receptor alpha gene .
1.1380 30.1405 0.9999 In order to further understand the mechanisms directing the expression of these key regulators of hematopoiesis , we initiated a study investigating the proteintranscription factors activating the expression of the granulocyte-macrophage colony-stimulating factor ( GM-CSF ) receptor alpha gene .
0.9537 1.0000 0.9974 In order to further understand the mechanisms directing the expression of these key regulators of hematopoiesis , we initiated a study investigating the transcription factors activating the expression of the granulocyte-macrophage colony-stimulating factor ( proteinGM-CSF ) receptor alpha gene .
0.8283 0.8203 0.9140 In order to further understand the mechanisms directing the expression of these key regulators of hematopoiesis , we initiated a study investigating the transcription factors activating the expression of the DNAgranulocyte-macrophage colony-stimulating factor ( GM-CSF ) receptor alpha gene .
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5.6513 30.7659 20.6696 Here, we demonstrate that the DNAhuman GM-CSF receptor alpha promoter directs reporter gene activity in a tissue-specific fashion in myelomonocytic cells , which correlates with its expression pattern as analyzed by reverse transcription PCR .
1.9491 20.1137 0.9998 Here, we demonstrate that the human GM-CSF receptor alpha promoter directs reporter gene activity in a tissue-specific fashion in cell_typemyelomonocytic cells , which correlates with its expression pattern as analyzed by reverse transcription PCR .
0.9197 1.0000 0.9970 Here, we demonstrate that the human proteinGM-CSF receptor alpha promoter directs reporter gene activity in a tissue-specific fashion in myelomonocytic cells , which correlates with its expression pattern as analyzed by reverse transcription PCR .
Here, we demonstrate that the human GM-CSF receptor alpha promoter directs DNAreporter gene activity in a tissue-specific fashion in myelomonocytic cells , which correlates with its expression pattern as analyzed by reverse transcription PCR .
Here, we demonstrate that the human proteinGM-CSF receptor alpha promoter directs reporter gene activity in a tissue-specific fashion in myelomonocytic cells , which correlates with its expression pattern as analyzed by reverse transcription PCR .
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3.2993 10.8695 10.8067 The DNAGM-CSF receptor alpha promoter contains an important functional site between positions -53 and -41 as identified by deletion analysis of reporter constructs .
1.3249 10.9682 0.9998 The GM-CSF receptor alpha promoter contains an important functional site between positions -53 and -41 as identified by deletion analysis of DNAreporter constructs .
0.7469 1.0000 0.9964 The proteinGM-CSF receptor alpha promoter contains an important functional site between positions -53 and -41 as identified by deletion analysis of reporter constructs .
0.5677 0.9979 10.5777 The proteinGM-CSF receptor alpha promoter contains an important functional site between positions -53 and -41 as identified by deletion analysis of reporter constructs .
3.4849 20.2775 10.8279 The GM-CSF receptor alpha promoter contains an important functional site between DNApositions -53 and -41 as identified by deletion analysis of reporter constructs .
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0.9315 0.9997 0.9999 We show that the myeloid and B cell transcription factor proteinPU.1 binds specifically to this site.
6.3153 30.5808 10.8603 We show that the proteinmyeloid and B cell transcription factor PU.1 binds specifically to this site.
0.5990 0.9562 0.9996 We show that the myeloid and B cell proteintranscription factor PU.1 binds specifically to this site.
We show that the myeloid and proteinB cell transcription factor PU.1 binds specifically to this site.
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3.4620 20.7380 10.9954 Furthermore, we demonstrate that a CCAAT site located upstream of the PU.1 site between positions -70 and -54 is involved in positive-negative regulation of the proteinGM-CSF receptor alpha promoter activity .
2.2153 20.1100 0.9968 Furthermore, we demonstrate that a CCAAT site located upstream of the PU.1 site between positions -70 and -54 is involved in positive-negative regulation of the proteinGM-CSF receptor alpha promoter activity .
2.0955 20.0814 1.0000 Furthermore, we demonstrate that a CCAAT site located upstream of the DNAPU.1 site between positions -70 and -54 is involved in positive-negative regulation of the GM-CSF receptor alpha promoter activity .
2.0955 20.1109 0.9999 Furthermore, we demonstrate that a DNACCAAT site located upstream of the PU.1 site between positions -70 and -54 is involved in positive-negative regulation of the GM-CSF receptor alpha promoter activity .
2.0515 20.0661 0.9947 Furthermore, we demonstrate that a CCAAT site located upstream of the proteinPU.1 site between positions -70 and -54 is involved in positive-negative regulation of the GM-CSF receptor alpha promoter activity .
2.9266 10.8897 10.6532 Furthermore, we demonstrate that a CCAAT site located upstream of the PU.1 site between positions DNA-70 and -54 is involved in positive-negative regulation of the GM-CSF receptor alpha promoter activity .
Furthermore, we demonstrate that a CCAAT site located upstream of the PU.1 site between positions -70 and -54 is involved in positive-negative regulation of the DNAGM-CSF receptor alpha promoter activity .
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3.4912 20.2909 10.6733 C/EBP alpha is the major proteinCCAAT/enhancer -binding protein ( C/EBP ) form binding to this site in nuclear extracts of U937 cells .
2.2266 20.4234 0.9999 C/EBP alpha is the major CCAAT/enhancer -binding protein ( C/EBP ) form binding to this site in nuclear extracts of cell_lineU937 cells .
0.9080 1.0000 1.0000 proteinC/EBP alpha is the major CCAAT/enhancer -binding protein ( C/EBP ) form binding to this site in nuclear extracts of U937 cells .
0.7997 1.0000 0.9987 C/EBP alpha is the major CCAAT/enhancer -binding protein ( proteinC/EBP ) form binding to this site in nuclear extracts of U937 cells .
1.4375 10.5747 0.9997 C/EBP alpha is the major CCAAT/enhancer -binding protein ( proteinC/EBP ) form binding to this site in nuclear extracts of U937 cells .
C/EBP alpha is the major DNACCAAT/enhancer -binding protein ( C/EBP ) form binding to this site in nuclear extracts of U937 cells .
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3.5015 20.7311 10.8702 Point mutations of either the PU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of proteinGM-CSF receptor alpha promoter activity in myelomonocytic cells only.
2.1907 20.6894 0.9998 Point mutations of either the PU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of DNAGM-CSF receptor alpha promoter activity in myelomonocytic cells only.
1.9865 20.2238 0.9993 Point mutations of either the PU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of GM-CSF receptor alpha promoter activity in cell_typemyelomonocytic cells only.
1.4093 10.9541 0.9999 Point mutations of either the DNAPU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of GM-CSF receptor alpha promoter activity in myelomonocytic cells only.
1.3669 10.9967 0.9998 Point mutations of either the PU.1 site or the DNAC/EBP site that abolish the binding of the respective factors result in a significant decrease of GM-CSF receptor alpha promoter activity in myelomonocytic cells only.
0.7745 1.0000 0.9977 Point mutations of either the PU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of proteinGM-CSF receptor alpha promoter activity in myelomonocytic cells only.
Point mutations of either the proteinPU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of GM-CSF receptor alpha promoter activity in myelomonocytic cells only.
Point mutations of either the PU.1 site or the proteinC/EBP site that abolish the binding of the respective factors result in a significant decrease of GM-CSF receptor alpha promoter activity in myelomonocytic cells only.
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2.4042 20.5605 10.5063 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the DNAGM-CSF receptor alpha promoter PU.1 site .
1.4752 20.5590 10.4118 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the proteinGM-CSF receptor alpha promoter PU.1 site .
0.9621 1.0000 1.0000 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( proteinPU-SF ) when binding the GM-CSF receptor alpha promoter PU.1 site .
0.9551 0.9999 0.9389 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the GM-CSF receptor alpha promoter proteinPU.1 site .
0.8684 1.0000 1.0000 Furthermore, we demonstrate that in myeloid and B cell extracts , proteinPU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the GM-CSF receptor alpha promoter PU.1 site .
0.7852 0.9659 0.9994 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the GM-CSF receptor alpha promoter DNAPU.1 site .
0.6377 1.0000 0.9945 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the proteinGM-CSF receptor alpha promoter PU.1 site .
4.5246 20.5094 10.8872 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more proteinslowly migrating complex ( PU-SF ) when binding the GM-CSF receptor alpha promoter PU.1 site .
4.2680 20.4712 10.7649 Furthermore, we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel, specific, more slowly migrating complex ( PU-SF ) when binding the DNAGM-CSF receptor alpha promoter PU.1 site .
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4.6490 20.6656 10.8942 This is the first demonstration of a specific interaction with PU.1 on a DNAmyeloid PU.1 binding site .
1.3044 10.8926 1.0000 This is the first demonstration of a specific interaction with proteinPU.1 on a myeloid PU.1 binding site .
0.8880 1.0000 0.9943 This is the first demonstration of a specific interaction with PU.1 on a myeloid proteinPU.1 binding site .
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4.3334 20.8054 10.9362 The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of PU.1 to extracts from certain cell_typenonmyeloid cell types which do not express PU.1 , including T cells and epithelial cells , but not from erythroid cells .
4.0469 20.8599 10.5486 The novel complex is distinct from that described previously as binding to DNAB cell enhancer sites and can be formed by addition of PU.1 to extracts from certain nonmyeloid cell types which do not express PU.1 , including T cells and epithelial cells , but not from erythroid cells .
2.2006 20.4228 0.9998 The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of PU.1 to extracts from certain nonmyeloid cell types which do not express PU.1 , including T cells and epithelial cells , but not from cell_typeerythroid cells .
1.6702 10.0324 1.0000 The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of PU.1 to extracts from certain nonmyeloid cell types which do not express proteinPU.1 , including T cells and epithelial cells , but not from erythroid cells .
1.6603 10.1799 1.0000 The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of proteinPU.1 to extracts from certain nonmyeloid cell types which do not express PU.1 , including T cells and epithelial cells , but not from erythroid cells .
1.5655 10.7862 0.9999 The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of PU.1 to extracts from certain nonmyeloid cell types which do not express PU.1 , including T cells and cell_typeepithelial cells , but not from erythroid cells .
1.5198 10.9067 0.9999 The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of PU.1 to extracts from certain nonmyeloid cell types which do not express PU.1 , including cell_typeT cells and epithelial cells , but not from erythroid cells .
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2.2402 20.5235 0.9999 Furthermore, we demonstrate that the proteinPU-SF complex binds to PU.1 sites found on a number of myeloid promoters , and its formation requires an intact PU.1 site adjacent to a single-stranded region.
2.1655 20.2695 1.0000 Furthermore, we demonstrate that the PU-SF complex binds to PU.1 sites found on a number of myeloid promoters , and its formation requires an intact DNAPU.1 site adjacent to a single-stranded region.
2.1087 20.0512 0.9999 Furthermore, we demonstrate that the PU-SF complex binds to PU.1 sites found on a number of DNAmyeloid promoters , and its formation requires an intact PU.1 site adjacent to a single-stranded region.
2.0602 20.0445 0.9902 Furthermore, we demonstrate that the PU-SF complex binds to PU.1 sites found on a number of myeloid promoters , and its formation requires an intact proteinPU.1 site adjacent to a single-stranded region.
1.6020 20.5005 0.9727 Furthermore, we demonstrate that the proteinPU-SF complex binds to PU.1 sites found on a number of myeloid promoters , and its formation requires an intact PU.1 site adjacent to a single-stranded region.
1.5183 10.8961 0.9940 Furthermore, we demonstrate that the PU-SF complex binds to proteinPU.1 sites found on a number of myeloid promoters , and its formation requires an intact PU.1 site adjacent to a single-stranded region.
2.2345 20.0170 1.0000 Furthermore, we demonstrate that the PU-SF complex binds to DNAPU.1 sites found on a number of myeloid promoters , and its formation requires an intact PU.1 site adjacent to a single-stranded region.
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2.9860 20.7186 10.1118 Expression of PU.1 in nonmyeloid cells can activate the DNAGM-CSF receptor alpha promoter .
2.0402 20.1836 0.9962 Expression of PU.1 in nonmyeloid cells can activate the proteinGM-CSF receptor alpha promoter .
1.2922 10.9737 1.0000 Expression of proteinPU.1 in nonmyeloid cells can activate the GM-CSF receptor alpha promoter .
1.2743 10.7631 0.9997 Expression of PU.1 in cell_typenonmyeloid cells can activate the GM-CSF receptor alpha promoter .
2.2520 20.4517 10.8480 Expression of PU.1 in nonmyeloid cells can activate the proteinGM-CSF receptor alpha promoter .
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3.9561 20.8669 10.6937 Deletion of the amino-terminal region of PU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the PU-SF complex is of functional importance for the activity of the DNAGM-CSF receptor alpha promoter .
2.2571 20.4164 1.0000 Deletion of the amino-terminal region of PU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the proteinPU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter .
2.1507 20.5913 1.0000 Deletion of the proteinamino-terminal region of PU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the PU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter .
1.7307 20.9040 0.9850 Deletion of the amino-terminal region of PU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the proteinPU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter .
1.4981 10.0782 0.9978 Deletion of the amino-terminal region of PU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the PU-SF complex is of functional importance for the activity of the proteinGM-CSF receptor alpha promoter .
0.8762 1.0000 1.0000 Deletion of the amino-terminal region of proteinPU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the PU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter .
2.2962 20.1235 1.0000 Deletion of the amino-terminal region of PU.1 results in a failure to form the proteinPU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the PU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter .
Deletion of the amino-terminal region of PU.1 results in a failure to form the proteinPU-SF complex and in a concomitant loss of transactivation, suggesting that formation of the PU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter .
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2.4330 10.8739 10.4353 Finally, we demonstrate that C/EBP alpha can also active the DNAGM-CSF receptor alpha promoter in nonmyeloid cells .
1.4377 10.1052 0.9994 Finally, we demonstrate that C/EBP alpha can also active the GM-CSF receptor alpha promoter in cell_typenonmyeloid cells .
1.3822 10.4029 0.9999 Finally, we demonstrate that proteinC/EBP alpha can also active the GM-CSF receptor alpha promoter in nonmyeloid cells .
0.6899 1.0000 0.9977 Finally, we demonstrate that C/EBP alpha can also active the proteinGM-CSF receptor alpha promoter in nonmyeloid cells .
Finally, we demonstrate that proteinC/EBP alpha can also active the GM-CSF receptor alpha promoter in nonmyeloid cells .
Finally, we demonstrate that C/EBP alpha can also active the proteinGM-CSF receptor alpha promoter in nonmyeloid cells .
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1.4770 10.6439 1.0000 HMG-I binds to DNAGATA motifs : implications for an HPFH syndrome .
0.9690 1.0000 1.0000 proteinHMG-I binds to GATA motifs : implications for an HPFH syndrome .
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3.4520 20.2876 10.5573 We have examined binding of the nuclear protein HMG-I to the DNAhuman gamma-globin promoter .
1.6463 20.3886 0.9841 We have examined binding of the proteinnuclear protein HMG-I to the human gamma-globin promoter .
0.9852 1.0000 1.0000 We have examined binding of the nuclear protein proteinHMG-I to the human gamma-globin promoter .
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2.8490 30.4582 10.7462 We find that HMG-I binds preferentially to the more 3' of a pair of GATA motifs in the gamma-globin promoter ; this paired motif is bound by the proteinerythroid factor GATA-1 .
2.1494 20.7070 0.9999 We find that HMG-I binds preferentially to the more 3' of a pair of DNAGATA motifs in the gamma-globin promoter ; this paired motif is bound by the erythroid factor GATA-1 .
2.1231 20.1361 0.9999 We find that HMG-I binds preferentially to the more 3' of a pair of GATA motifs in the DNAgamma-globin promoter ; this paired motif is bound by the erythroid factor GATA-1 .
1.7438 10.0494 1.0000 We find that proteinHMG-I binds preferentially to the more 3' of a pair of GATA motifs in the gamma-globin promoter ; this paired motif is bound by the erythroid factor GATA-1 .
0.9522 1.0000 1.0000 We find that HMG-I binds preferentially to the more 3' of a pair of GATA motifs in the gamma-globin promoter ; this paired motif is bound by the erythroid factor proteinGATA-1 .
2.0759 20.2015 0.9999 We find that HMG-I binds preferentially to the more 3' of a pair of GATA motifs in the gamma-globin promoter ; this DNApaired motif is bound by the erythroid factor GATA-1 .
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3.9014 20.7497 10.4402 A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of gamma-globin in cell_typeadult red blood cells ( HPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence .
2.2196 20.6383 0.9999 A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of gamma-globin in adult red blood cells ( HPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this DNAmutant sequence .
2.1922 20.6688 1.0000 A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of gamma-globin in adult red blood cells ( HPFH ) and up-regulation of the DNAgamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence .
1.6620 10.1948 1.0000 A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of proteingamma-globin in adult red blood cells ( HPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence .
0.9371 1.0000 1.0000 A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of gamma-globin in adult red blood cells ( cell_typeHPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence .
0.8822 1.0000 1.0000 A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of gamma-globin in adult red blood cells ( HPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; proteinHMG-I does not bind to this mutant sequence .
0.8316 1.0000 1.0000 A naturally occurring mutation (-175 T-C) in the area bound by proteinHMG-I results in overexpression of gamma-globin in adult red blood cells ( HPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence .
A naturally occurring mutation (-175 T-C) in the area bound by HMG-I results in overexpression of gamma-globin in adult red blood cells ( HPFH ) and up-regulation of the proteingamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence .
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2.1028 20.1677 1.0000 A survey of DNAGATA motifs from other globin cis-elements demonstrates HMG-I binding to most of them.
1.4410 10.9345 0.9999 A survey of GATA motifs from other DNAglobin cis-elements demonstrates HMG-I binding to most of them.
0.9189 1.0000 1.0000 A survey of GATA motifs from other globin cis-elements demonstrates proteinHMG-I binding to most of them.
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2.3546 20.3693 1.0000 These findings implicate HMG-I in the HPFH phenotype ; we speculate that it may participate in the formation of proteinmultiprotein complexes that regulate globin gene expression .
1.7634 10.5016 1.0000 These findings implicate proteinHMG-I in the HPFH phenotype ; we speculate that it may participate in the formation of multiprotein complexes that regulate globin gene expression .
2.3566 20.0540 0.9997 These findings implicate HMG-I in the HPFH phenotype ; we speculate that it may participate in the formation of multiprotein complexes that regulate DNAglobin gene expression .
These findings implicate HMG-I in the cell_typeHPFH phenotype ; we speculate that it may participate in the formation of multiprotein complexes that regulate globin gene expression .
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2.1793 30.6902 10.6695 Constitutive activation of different proteinJak tyrosine kinases in human T cell leukemia virus type 1 ( HTLV-1 ) tax protein or virus-transformed cells .
1.8723 20.8938 0.9991 Constitutive activation of different Jak tyrosine kinases in human T cell leukemia virus type 1 ( HTLV-1 ) tax protein or cell_linevirus-transformed cells .
1.6561 0.9370 20.2882 Constitutive activation of different Jak tyrosine kinases in proteinhuman T cell leukemia virus type 1 ( HTLV-1 ) tax protein or virus-transformed cells .
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3.0156 10.9205 10.7559 The proteinviral encoded protein tax , is thought to play an important role in oncogenesis .
0.9811 1.0000 1.0000 The viral encoded protein proteintax , is thought to play an important role in oncogenesis .
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1.7494 10.4389 1.0000 Our previous data obtained from a tax transgenic mouse model revealed that tax transforms mouse fibroblasts but not cell_typethymocytes , despite comparable levels of tax expression in both tissues.
1.7360 10.0484 1.0000 Our previous data obtained from a tax transgenic mouse model revealed that proteintax transforms mouse fibroblasts but not thymocytes , despite comparable levels of tax expression in both tissues.
1.6787 10.4494 1.0000 Our previous data obtained from a tax transgenic mouse model revealed that tax transforms mouse fibroblasts but not thymocytes , despite comparable levels of proteintax expression in both tissues.
1.6266 10.2960 1.0000 Our previous data obtained from a proteintax transgenic mouse model revealed that tax transforms mouse fibroblasts but not thymocytes , despite comparable levels of tax expression in both tissues.
1.5578 10.5678 0.9999 Our previous data obtained from a tax transgenic mouse model revealed that tax transforms cell_typemouse fibroblasts but not thymocytes , despite comparable levels of tax expression in both tissues.
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6.2676 30.4707 20.3635 Constitutive tyrosine phosphorylation of a 130-kD protein (s) was observed in the tax transformed fibroblast B line and in cell_lineHTLV-1 transformed human lymphoid lines , but not in thymocytes from Thy-tax transgenic mice .
1.9327 20.9141 1.0000 Constitutive tyrosine phosphorylation of a protein130-kD protein (s) was observed in the tax transformed fibroblast B line and in HTLV-1 transformed human lymphoid lines , but not in thymocytes from Thy-tax transgenic mice .
1.5632 10.1191 1.0000 Constitutive tyrosine phosphorylation of a 130-kD protein (s) was observed in the tax transformed fibroblast B line and in HTLV-1 transformed human lymphoid lines , but not in cell_typethymocytes from Thy-tax transgenic mice .
5.4078 20.9456 20.9862 Constitutive tyrosine phosphorylation of a 130-kD protein (s) was observed in the cell_linetax transformed fibroblast B line and in HTLV-1 transformed human lymphoid lines , but not in thymocytes from Thy-tax transgenic mice .
Constitutive tyrosine phosphorylation of a 130-kD protein (s) was observed in the proteintax transformed fibroblast B line and in HTLV-1 transformed human lymphoid lines , but not in thymocytes from Thy-tax transgenic mice .
Constitutive tyrosine phosphorylation of a 130-kD protein (s) was observed in the tax cell_linetransformed fibroblast B line and in HTLV-1 transformed human lymphoid lines , but not in thymocytes from Thy-tax transgenic mice .
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7.0562 40.6808 20.5174 Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as Jak2 in the tax transformed mouse fibroblastic cell line and Jak3 in cell_lineHTLV-1 transformed human T cell lines .
5.0047 30.3447 10.4925 Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of proteinJak kinase specific antibodies , identified p130 as Jak2 in the tax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
0.8596 0.9999 1.0000 Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as proteinJak2 in the tax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
0.8488 0.9997 1.0000 Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as Jak2 in the tax transformed mouse fibroblastic cell line and proteinJak3 in HTLV-1 transformed human T cell lines .
7.7758 30.9470 20.7674 Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as Jak2 in the cell_linetax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
0.8714 1.0000 1.0000 Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified proteinp130 as Jak2 in the tax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as Jak2 in the tax transformed cell_linemouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of proteinJak kinase specific antibodies , identified p130 as Jak2 in the tax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as Jak2 in the proteintax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines .
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2.9299 10.7911 10.9690 Phosphorylation of Jak2 in cell_linetax transformed cells resulted from high expression of IL-6 .
1.3401 10.8170 1.0000 Phosphorylation of Jak2 in tax transformed cells resulted from high expression of proteinIL-6 .
1.2927 10.7931 1.0000 Phosphorylation of proteinJak2 in tax transformed cells resulted from high expression of IL-6 .
Phosphorylation of Jak2 in proteintax transformed cells resulted from high expression of IL-6 .
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2.5067 20.0544 0.9999 Tyrosine phosphorylation of this protein could also be induced in Balb/c3T3 cells using a supernatant from the cell_lineB line , which was associated with induction of cell proliferation .
2.4561 20.6760 1.0000 Tyrosine phosphorylation of this protein could also be induced in cell_lineBalb/c3T3 cells using a supernatant from the B line , which was associated with induction of cell proliferation .
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2.7752 20.0276 10.7567 Both phosphorylation and proliferation were inhibited by proteinIL-6 neutralizing antibodies .
1.3265 10.4001 0.9957 Both phosphorylation and proliferation were inhibited by proteinIL-6 neutralizing antibodies .
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6.4270 30.4610 20.0919 Constitutive phosphorylation of Jak kinases may facilitate tumor growth in both cell_typeHTLV-1 infected human T cells and the transgenic mouse model .
1.2288 20.3922 1.0000 Constitutive phosphorylation of proteinJak kinases may facilitate tumor growth in both HTLV-1 infected human T cells and the transgenic mouse model .
Constitutive phosphorylation of Jak kinases may facilitate tumor growth in both HTLV-1 infected human cell_typeT cells and the transgenic mouse model .
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3.9750 20.5186 10.9307 Regulation of c-jun mRNA expression by hydroxyurea in cell_linehuman K562 cells during erythroid differentiation [published erratum appears in Biochim Biophys Acta 1995 Dec 27;1264(3):409]
2.4792 20.4352 0.9999 Regulation of RNAc-jun mRNA expression by hydroxyurea in human K562 cells during erythroid differentiation [published erratum appears in Biochim Biophys Acta 1995 Dec 27;1264(3):409]
Regulation of DNAc-jun mRNA expression by hydroxyurea in human K562 cells during erythroid differentiation [published erratum appears in Biochim Biophys Acta 1995 Dec 27;1264(3):409]
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2.2858 20.4164 1.0000 In addition, HU stimulates the synthesis of proteinfetal hemoglobin in sickle cell anemia patients .
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2.4410 20.7089 0.9999 To further understand its mechanism of action, we investigated the effects of HU on regulation of c-jun expression prior to the onset of erythroid differentiation of cell_lineK562 cells .
1.7795 10.5043 1.0000 To further understand its mechanism of action, we investigated the effects of HU on regulation of DNAc-jun expression prior to the onset of erythroid differentiation of K562 cells .
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1.5309 10.4101 1.0000 HU induced a dose-dependent stimulation of DNAc-jun synthesis.
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2.4887 20.2082 1.0000 The levels of RNAc-jun mRNA was elevated 4 to 7.5-fold by HU within 2 h.
1.5224 20.3445 0.9906 The levels of DNAc-jun mRNA was elevated 4 to 7.5-fold by HU within 2 h.
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2.5351 20.9629 1.0000 Both nuclear run-on and actinomycin D pulse experiments strongly indicate that HU regulates c-jun mRNA expression by increasing the rate of synthesis as well as stabilizing the RNAc-jun mRNA .
1.7310 10.6208 1.0000 Both nuclear run-on and actinomycin D pulse experiments strongly indicate that HU regulates RNAc-jun mRNA expression by increasing the rate of synthesis as well as stabilizing the c-jun mRNA .
0.8837 1.0000 1.0000 Both nuclear run-on and actinomycin D pulse experiments strongly indicate that proteinHU regulates c-jun mRNA expression by increasing the rate of synthesis as well as stabilizing the c-jun mRNA .
Both nuclear run-on and actinomycin D pulse experiments strongly indicate that HU regulates c-jun mRNA expression by increasing the rate of synthesis as well as stabilizing the DNAc-jun mRNA .
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2.2065 20.6051 1.0000 In addition, the level of proteinjun protein was elevated by 2 to 5-fold within 4 h in HU treated cells .
1.9141 20.9866 10.6173 In addition, the level of jun protein was elevated by 2 to 5-fold within 4 h in cell_lineHU treated cells .
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0.9574 1.0000 0.9998 Furthermore, concentrations of HU below 250 microM slightly increased the 5X AP-1 protein/CAT activity .
1.5887 20.4182 0.9926 Furthermore, concentrations of HU below 250 microM slightly increased the protein5X AP-1 /CAT activity .
Furthermore, concentrations of HU below 250 microM slightly increased the 5X proteinAP-1 /CAT activity .
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1.6843 10.4793 1.0000 These results strongly suggest that HU induces both transcriptional and post-transcription regulation of DNAc-jun during erythroid differentiation .
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2.2998 20.2795 1.0000 In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in man : relationship to proteinglucocorticoid receptors .
0.9129 1.0000 1.0000 In vivo and in vitro effects of glucocorticoids on cell_typelymphocyte proliferation in man : relationship to glucocorticoid receptors .
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1.6935 10.5115 1.0000 While in vitro administration of glucocorticoids may inhibit concanavalin A (Con A)- and phytohemagglutinin (PHA)- induced T-cell proliferation , proteinpokeweed mitogen ( PWM )-driven B-cell mitogenesis is relatively resistant to glucocorticoids .
0.9866 1.0000 1.0000 While in vitro administration of glucocorticoids may inhibit concanavalin A (Con A)- and phytohemagglutinin (PHA)- induced T-cell proliferation , pokeweed mitogen ( proteinPWM )-driven B-cell mitogenesis is relatively resistant to glucocorticoids .
0.8704 1.0000 1.0000 While in vitro administration of glucocorticoids may inhibit concanavalin A (Con A)- and proteinphytohemagglutinin (PHA)- induced T-cell proliferation , pokeweed mitogen ( PWM )-driven B-cell mitogenesis is relatively resistant to glucocorticoids .
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1.8789 10.0656 1.0000 To further explore the link between the HPA and the immune system in relation to glucocorticoid receptor function , dose-response curves were obtained for Con A -and proteinPHA -induced T-cell mitogenesis , PWM -generated B-cell mitogenesis and spontaneous lymphocyte proliferation in 13 healthy controls .
1.7184 10.8266 1.0000 To further explore the link between the HPA and the immune system in relation to proteinglucocorticoid receptor function , dose-response curves were obtained for Con A -and PHA -induced T-cell mitogenesis , PWM -generated B-cell mitogenesis and spontaneous lymphocyte proliferation in 13 healthy controls .
0.9522 1.0000 1.0000 To further explore the link between the HPA and the immune system in relation to glucocorticoid receptor function , dose-response curves were obtained for Con A -and PHA -induced T-cell mitogenesis , proteinPWM -generated B-cell mitogenesis and spontaneous lymphocyte proliferation in 13 healthy controls .
0.5482 0.9999 1.0000 To further explore the link between the HPA and the immune system in relation to glucocorticoid receptor function , dose-response curves were obtained for Con A -and PHA -induced T-cell mitogenesis , PWM -generated cell_typeB-cell mitogenesis and spontaneous lymphocyte proliferation in 13 healthy controls .
0.5149 1.0000 1.0000 To further explore the link between the HPA and the immune system in relation to glucocorticoid receptor function , dose-response curves were obtained for Con A -and PHA -induced T-cell mitogenesis , PWM -generated B-cell mitogenesis and spontaneous cell_typelymphocyte proliferation in 13 healthy controls .
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1.8780 10.0352 1.0000 There was a significant decrease in proteinPWM -induced B-cell mitogenesis and a more pronounced effect of DEX administered in vitro on spontaneous lymphocyte proliferation after MET treatment when compared with the DEX plus MET pretreated condition in vivo.
0.9051 1.0000 1.0000 There was a significant decrease in PWM -induced cell_typeB-cell mitogenesis and a more pronounced effect of DEX administered in vitro on spontaneous lymphocyte proliferation after MET treatment when compared with the DEX plus MET pretreated condition in vivo.
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2.3570 20.2602 1.0000 These data suggest that the inhibition of spontaneous lymphocyte proliferation by glucocorticoids in vitro is related to proteinglucocorticoid receptor function .
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1.7222 10.2264 1.0000 The decrease in proteinPWM -generated B-cell proliferation following cortisol depletion by MET may be seen in connection with impaired glucocorticoid -mediated induction of interleukin-1 receptor synthesis .
1.4622 10.8625 1.0000 The decrease in PWM -generated B-cell proliferation following cortisol depletion by MET may be seen in connection with impaired glucocorticoid -mediated induction of proteininterleukin-1 receptor synthesis .
1.9936 20.0953 0.9919 The decrease in PWM -generated B-cell proliferation following cortisol depletion by MET may be seen in connection with impaired glucocorticoid -mediated induction of proteininterleukin-1 receptor synthesis .
0.9209 0.9999 1.0000 The decrease in PWM -generated cell_typeB-cell proliferation following cortisol depletion by MET may be seen in connection with impaired glucocorticoid -mediated induction of interleukin-1 receptor synthesis .
0.8277 1.0000 1.0000 The decrease in PWM -generated B-cell proliferation following cortisol depletion by proteinMET may be seen in connection with impaired glucocorticoid -mediated induction of interleukin-1 receptor synthesis .
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4.0076 20.9523 10.4561 Application of a "formamide free" and thus "material preserving" in situ hybridization technique using the cDNA of the myf3 gene revealed the following results: cell_typeHuman rhabdomyosarcoma cells , characterized by a high expression of myf3 show intensive hybridization signals in their interphase .
1.7071 10.2254 1.0000 Application of a "formamide free" and thus "material preserving" in situ hybridization technique using the DNAcDNA of the myf3 gene revealed the following results: Human rhabdomyosarcoma cells , characterized by a high expression of myf3 show intensive hybridization signals in their interphase .
1.5400 10.4266 1.0000 Application of a "formamide free" and thus "material preserving" in situ hybridization technique using the cDNA of the DNAmyf3 gene revealed the following results: Human rhabdomyosarcoma cells , characterized by a high expression of myf3 show intensive hybridization signals in their interphase .
1.5450 10.9271 1.0000 Application of a "formamide free" and thus "material preserving" in situ hybridization technique using the cDNA of the myf3 gene revealed the following results: Human rhabdomyosarcoma cells , characterized by a high expression of proteinmyf3 show intensive hybridization signals in their interphase .
Application of a "formamide free" and thus "material preserving" in situ hybridization technique using the cDNA of the myf3 gene revealed the following results: Human rhabdomyosarcoma cells , characterized by a high expression of DNAmyf3 show intensive hybridization signals in their interphase .
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0.9856 1.0000 1.0000 proteinRNase treatment prior to hybridization considerably reduces the size of this signals.
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2.4630 20.1512 1.0000 In comparison, isolated nuclei of cell_typehuman lymphocytes in which no need for the expression of this gene exists, show barely hybridization signals .
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0.9304 1.0000 1.0000 Correspondingly, proteinRNase treatment had no effect on hybridization pattern at all.
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4.0814 20.9607 10.7871 In conclusion an increased transcription efficiency of a DNAcell type specific gene is accompanied by a higher hybridization accessibility in the corresponding cell nuclei .
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3.5604 20.9420 10.3620 Oncogenicity of human papillomavirus- or adenovirus- transformed cells correlates with resistance to lysis by cell_typenatural killer cells .
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5.1998 20.9430 10.6696 The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the E1A and E7 proteins to target cells for rejection by the host cell_typenatural killer (NK) cell response .
The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the E1A and E7 proteins to cell_typetarget cells for rejection by the host natural killer (NK) cell response .
The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the proteinE1A and E7 proteins to target cells for rejection by the host natural killer (NK) cell response .
The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the E1A and E7 proteins to target cells for rejection by the cell_typehost natural killer (NK) cell response .
The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the E1A and proteinE7 proteins to target cells for rejection by the host natural killer (NK) cell response .
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2.2098 10.6183 10.9026 As one test of this hypothesis, we compared the abilities of E1A -and E7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either unstimulated or cell_lineinterferon (IFN)-activated NK cells .
0.9041 1.0000 1.0000 As one test of this hypothesis, we compared the abilities of E1A -and proteinE7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either unstimulated or interferon (IFN)-activated NK cells .
0.8876 1.0000 1.0000 As one test of this hypothesis, we compared the abilities of proteinE1A -and E7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either unstimulated or interferon (IFN)-activated NK cells .
3.0168 10.8487 10.9675 As one test of this hypothesis, we compared the abilities of E1A -and E7 -expressing human fibroblastic or cell_typekeratinocyte-derived human cells to be selectively killed by either unstimulated or interferon (IFN)-activated NK cells .
0.7951 0.9978 0.9991 As one test of this hypothesis, we compared the abilities of E1A -and E7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either unstimulated or interferon (IFN)-activated cell_typeNK cells .
0.5079 1.0000 0.9934 As one test of this hypothesis, we compared the abilities of E1A -and E7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either unstimulated or proteininterferon (IFN)-activated NK cells .
As one test of this hypothesis, we compared the abilities of E1A -and E7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either cell_typeunstimulated or interferon (IFN)-activated NK cells .
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2.3368 20.8191 1.0000 Cells expressing the proteinE1A oncoprotein were selectively killed by unstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 E7 oncoprotein were resistant to NK cell lysis .
1.1462 10.1626 1.0000 Cells expressing the E1A oncoprotein were selectively killed by unstimulated NK cells , while the same cell_typeparental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 E7 oncoprotein were resistant to NK cell lysis .
3.6644 20.7499 10.7346 Cells expressing the E1A oncoprotein were selectively killed by cell_typeunstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 E7 oncoprotein were resistant to NK cell lysis .
Cells expressing the E1A oncoprotein were selectively killed by unstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 proteinE7 oncoprotein were resistant to NK cell lysis .
Cells expressing the E1A oncoprotein were selectively killed by unstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 proteinE7 oncoprotein were resistant to NK cell lysis .
Cells expressing the E1A oncoprotein were selectively killed by cell_lineunstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 E7 oncoprotein were resistant to NK cell lysis .
Cells expressing the proteinE1A oncoprotein were selectively killed by unstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 E7 oncoprotein were resistant to NK cell lysis .
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3.4663 20.9972 10.9094 The ability of cell_lineIFN-activated NK cells to selectively kill virally transformed cells depends on IFN 's ability to induce resistance to NK cell lysis in normal (i.e., non-viral oncogene-expressing ) but not virally transformed cells .
2.3538 20.3481 10.8425 The ability of IFN-activated NK cells to selectively kill virally transformed cells depends on IFN 's ability to induce resistance to NK cell lysis in normal (i.e., non-viral oncogene-expressing ) but not cell_linevirally transformed cells .
0.9382 1.0000 1.0000 The ability of IFN-activated NK cells to selectively kill virally transformed cells depends on proteinIFN 's ability to induce resistance to NK cell lysis in normal (i.e., non-viral oncogene-expressing ) but not virally transformed cells .
3.3513 20.1732 10.9528 The ability of IFN-activated NK cells to selectively kill cell_linevirally transformed cells depends on IFN 's ability to induce resistance to NK cell lysis in normal (i.e., non-viral oncogene-expressing ) but not virally transformed cells .
0.7775 0.9998 0.9997 The ability of IFN-activated NK cells to selectively kill virally transformed cells depends on IFN 's ability to induce resistance to NK cell lysis in cell_typenormal (i.e., non-viral oncogene-expressing ) but not virally transformed cells .
The ability of IFN-activated NK cells to selectively kill virally transformed cells depends on IFN 's ability to induce resistance to NK cell lysis in normal (i.e., cell_linenon-viral oncogene-expressing ) but not virally transformed cells .
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2.5622 20.6219 10.2331 E1A blocked IFN 's induction of cytolytic resistance , resulting in the selective lysis of cell_lineadenovirus-transformed cells by IFN -activated NK cells .
1.3958 10.5412 0.9887 E1A blocked IFN 's induction of cytolytic resistance , resulting in the selective lysis of adenovirus-transformed cells by proteinIFN -activated NK cells .
0.9603 1.0000 1.0000 proteinE1A blocked IFN 's induction of cytolytic resistance , resulting in the selective lysis of adenovirus-transformed cells by IFN -activated NK cells .
0.9593 1.0000 1.0000 E1A blocked proteinIFN 's induction of cytolytic resistance , resulting in the selective lysis of adenovirus-transformed cells by IFN -activated NK cells .
2.1592 10.5784 10.5894 E1A blocked IFN 's induction of cytolytic resistance , resulting in the selective lysis of adenovirus-transformed cells by cell_typeIFN -activated NK cells .
E1A blocked IFN 's induction of cytolytic resistance , resulting in the selective lysis of adenovirus-transformed cells by cell_lineIFN -activated NK cells .
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3.9653 20.8628 10.7805 The extent of IFN -induced NK cell killing of cell_lineE1A -expressing cells was proportional to the level of E1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in target cells .
1.5313 20.3237 0.9946 The extent of IFN -induced NK cell killing of proteinE1A -expressing cells was proportional to the level of E1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in target cells .
1.3107 20.4418 0.9998 The extent of IFN -induced NK cell killing of E1A -expressing cells was proportional to the level of E1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in cell_typetarget cells .
0.9026 1.0000 1.0000 The extent of proteinIFN -induced NK cell killing of E1A -expressing cells was proportional to the level of E1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in target cells .
0.8972 1.0000 1.0000 The extent of IFN -induced NK cell killing of E1A -expressing cells was proportional to the level of E1A expression and correlated with the ability of E1A to block proteinIFN -stimulated gene expression in target cells .
0.8877 10.2681 1.0000 The extent of IFN -induced NK cell killing of E1A -expressing cells was proportional to the level of DNAE1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in target cells .
The extent of IFN -induced NK cell killing of E1A -expressing cells was proportional to the level of E1A expression and correlated with the ability of proteinE1A to block IFN -stimulated gene expression in target cells .
The extent of IFN -induced NK cell killing of E1A -expressing cells was proportional to the level of proteinE1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in target cells .
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3.8452 20.8799 10.6790 In contrast, E7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of cell_lineHPV -transformed cells by IFN -activated NK cells .
1.7153 10.8822 1.0000 In contrast, proteinE7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by IFN -activated NK cells .
1.6829 10.4969 1.0000 In contrast, E7 blocked neither proteinIFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by IFN -activated NK cells .
1.2998 10.5292 0.9794 In contrast, E7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by proteinIFN -activated NK cells .
0.9202 1.0000 1.0000 In contrast, E7 blocked neither IFN -stimulated gene expression nor proteinIFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by IFN -activated NK cells .
2.3869 10.5140 10.6827 In contrast, E7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by cell_typeIFN -activated NK cells .
1.6347 0.9999 10.2006 In contrast, E7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by IFN -activated cell_typeNK cells .
In contrast, E7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV -transformed cells by cell_lineIFN -activated NK cells .
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2.2384 20.3988 1.0000 In conclusion, E1A expression marks cells for destruction by the host NK cell response , whereas the proteinE7 oncoprotein lacks this activity.
2.1875 20.6965 0.9928 In conclusion, E1A expression marks cells for destruction by the host NK cell response , whereas the proteinE7 oncoprotein lacks this activity.
1.7196 10.8346 1.0000 In conclusion, DNAE1A expression marks cells for destruction by the host NK cell response , whereas the E7 oncoprotein lacks this activity.
In conclusion, E1A expression marks cells for destruction by the host cell_typeNK cell response , whereas the E7 oncoprotein lacks this activity.
In conclusion, proteinE1A expression marks cells for destruction by the host NK cell response , whereas the E7 oncoprotein lacks this activity.
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1.4821 10.6232 1.0000 Regulation of proteinIkB alpha phosphorylation by PKC- and Ca(2+)- dependent signal transduction pathways .
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4.3681 20.8003 10.4684 The Ca(2+) -dependent phosphatase calcineurin , a target of FK506 and CsA , synergizes with PKC -induced activation of proteinnuclear factor (NF)-kappa B in T cell lines .
3.5102 20.7153 10.5450 The Ca(2+) -dependent phosphatase calcineurin , a target of FK506 and CsA , synergizes with PKC -induced activation of nuclear factor (NF)-kappa B in cell_lineT cell lines .
2.8767 10.6984 10.3802 The proteinCa(2+) -dependent phosphatase calcineurin , a target of FK506 and CsA , synergizes with PKC -induced activation of nuclear factor (NF)-kappa B in T cell lines .
0.9342 1.0000 1.0000 The Ca(2+) -dependent phosphatase proteincalcineurin , a target of FK506 and CsA , synergizes with PKC -induced activation of nuclear factor (NF)-kappa B in T cell lines .
0.8747 0.9999 1.0000 The Ca(2+) -dependent phosphatase calcineurin , a target of FK506 and CsA , synergizes with proteinPKC -induced activation of nuclear factor (NF)-kappa B in T cell lines .
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2.4432 20.4925 1.0000 We have investigated whether this synergy is present in other cell types and the mechanism(s) by which these two pathways lead to proteinNF-kappa B activation .
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4.5997 20.6882 10.9546 While this synergy is present in other cell types, in the cell_linemonocytic cell line U937 calcineurin is also sufficient to activate NF-kappa B .
2.0216 20.0289 0.9999 While this synergy is present in other cell types, in the monocytic cell line U937 calcineurin is also sufficient to activate proteinNF-kappa B .
0.8944 1.0000 1.0000 While this synergy is present in other cell types, in the monocytic cell line U937 proteincalcineurin is also sufficient to activate NF-kappa B .
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2.3645 20.4898 1.0000 Having previously shown that Ca(2+)- and PKC- dependent pathways synergize by accelerating the degradation of IkB alpha , we focused on the regulation of proteinIkB alpha phosphorylation .
1.6126 10.9320 1.0000 Having previously shown that Ca(2+)- and PKC- dependent pathways synergize by accelerating the degradation of proteinIkB alpha , we focused on the regulation of IkB alpha phosphorylation .
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3.2779 10.8199 10.9652 While PKC -dependent pathways sequentially result in the phosphorylation and in an incomplete degradation of IkB alpha in cell_lineT cell lines , co-activation of Ca(2+) -dependent pathways accelerates the rate of IkB alpha phosphorylation and results in its complete degradation.
1.5700 10.7975 1.0000 While PKC -dependent pathways sequentially result in the phosphorylation and in an incomplete degradation of IkB alpha in T cell lines , co-activation of Ca(2+) -dependent pathways accelerates the rate of proteinIkB alpha phosphorylation and results in its complete degradation.
1.5510 10.8462 1.0000 While PKC -dependent pathways sequentially result in the phosphorylation and in an incomplete degradation of proteinIkB alpha in T cell lines , co-activation of Ca(2+) -dependent pathways accelerates the rate of IkB alpha phosphorylation and results in its complete degradation.
0.9583 1.0000 1.0000 While proteinPKC -dependent pathways sequentially result in the phosphorylation and in an incomplete degradation of IkB alpha in T cell lines , co-activation of Ca(2+) -dependent pathways accelerates the rate of IkB alpha phosphorylation and results in its complete degradation.
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2.2975 20.0537 1.0000 Activation of Ca(2+) -dependent pathways alone do not result in the phosphorylation and/or degradation of proteinIkB alpha in Jurkat T or in U937 cells .
1.6408 10.7523 0.9999 Activation of Ca(2+) -dependent pathways alone do not result in the phosphorylation and/or degradation of IkB alpha in cell_lineJurkat T or in U937 cells .
1.5900 10.6291 0.9998 Activation of Ca(2+) -dependent pathways alone do not result in the phosphorylation and/or degradation of IkB alpha in Jurkat T or in cell_lineU937 cells .
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2.4191 20.4187 0.9999 Treatment of cell_typeT cells with the selective PKC inhibitor GF109203X abrogates the PMA -induced IkB alpha phosphorylation /degradation irrespective of activation of Ca(2+) -dependent pathways , but not the phosphorylation and degradation of IkB alpha induced by TNF-alpha , a PKC -independent stimulus .
2.3665 20.1343 1.0000 Treatment of T cells with the selective PKC inhibitor GF109203X abrogates the PMA -induced IkB alpha phosphorylation /degradation irrespective of activation of Ca(2+) -dependent pathways , but not the phosphorylation and degradation of proteinIkB alpha induced by TNF-alpha , a PKC -independent stimulus .
1.7902 10.0386 1.0000 Treatment of T cells with the selective PKC inhibitor GF109203X abrogates the PMA -induced IkB alpha phosphorylation /degradation irrespective of activation of Ca(2+) -dependent pathways , but not the phosphorylation and degradation of IkB alpha induced by TNF-alpha , a proteinPKC -independent stimulus .
1.6848 10.3260 1.0000 Treatment of T cells with the selective PKC inhibitor GF109203X abrogates the PMA -induced IkB alpha phosphorylation /degradation irrespective of activation of Ca(2+) -dependent pathways , but not the phosphorylation and degradation of IkB alpha induced by proteinTNF-alpha , a PKC -independent stimulus .
1.6237 10.6345 0.9999 Treatment of T cells with the selective PKC inhibitor GF109203X abrogates the PMA -induced proteinIkB alpha phosphorylation /degradation irrespective of activation of Ca(2+) -dependent pathways , but not the phosphorylation and degradation of IkB alpha induced by TNF-alpha , a PKC -independent stimulus .
0.8764 1.0000 1.0000 Treatment of T cells with the selective proteinPKC inhibitor GF109203X abrogates the PMA -induced IkB alpha phosphorylation /degradation irrespective of activation of Ca(2+) -dependent pathways , but not the phosphorylation and degradation of IkB alpha induced by TNF-alpha , a PKC -independent stimulus .
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2.3784 20.3876 1.0000 Contrary to the interaction with PKC , Ca(2+) -dependent pathways synergize with TNF-alpha not at the level of proteinIkB alpha phosphorylation , but at the level of its degradation.
1.6334 10.4778 1.0000 Contrary to the interaction with PKC , Ca(2+) -dependent pathways synergize with proteinTNF-alpha not at the level of IkB alpha phosphorylation , but at the level of its degradation.
1.5840 10.7694 1.0000 Contrary to the interaction with proteinPKC , Ca(2+) -dependent pathways synergize with TNF-alpha not at the level of IkB alpha phosphorylation , but at the level of its degradation.
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2.4223 20.2074 1.0000 These results indicate that Ca(2+) -dependent pathways , including the phosphatase calcineurin , participate in the regulation of proteinNF-kappa B in a cell specific fashion and synergize with PKC -dependent and -independent pathways at the level of IkB alpha phosphorylation and degradation .
1.5891 10.7182 1.0000 These results indicate that Ca(2+) -dependent pathways , including the phosphatase calcineurin , participate in the regulation of NF-kappa B in a cell specific fashion and synergize with PKC -dependent and -independent pathways at the level of proteinIkB alpha phosphorylation and degradation .
0.9752 1.0000 1.0000 These results indicate that Ca(2+) -dependent pathways , including the phosphatase proteincalcineurin , participate in the regulation of NF-kappa B in a cell specific fashion and synergize with PKC -dependent and -independent pathways at the level of IkB alpha phosphorylation and degradation .
0.9197 1.0000 1.0000 These results indicate that Ca(2+) -dependent pathways , including the phosphatase calcineurin , participate in the regulation of NF-kappa B in a cell specific fashion and synergize with proteinPKC -dependent and -independent pathways at the level of IkB alpha phosphorylation and degradation .
0.8551 0.9993 1.0000 These results indicate that Ca(2+) -dependent pathways , including the proteinphosphatase calcineurin , participate in the regulation of NF-kappa B in a cell specific fashion and synergize with PKC -dependent and -independent pathways at the level of IkB alpha phosphorylation and degradation .
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3.8753 20.6778 10.8008 Vitamin E therapy of acute CCl4 -induced hepatic injury in mice is associated with inhibition of proteinnuclear factor kappa B binding .
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3.7116 20.6077 10.4748 Oxidative stress enhances proteinnuclear factor kappa B ( NF-kappa B ) activity , and NF-kappa B activity has been shown to enhance the expression of cytotoxic cytokines .
2.0407 20.8166 0.9999 Oxidative stress enhances nuclear factor kappa B ( NF-kappa B ) activity , and NF-kappa B activity has been shown to enhance the expression of proteincytotoxic cytokines .
1.4703 10.6474 0.9999 Oxidative stress enhances nuclear factor kappa B ( NF-kappa B ) activity , and proteinNF-kappa B activity has been shown to enhance the expression of cytotoxic cytokines .
0.8662 0.9999 0.9999 Oxidative stress enhances nuclear factor kappa B ( proteinNF-kappa B ) activity , and NF-kappa B activity has been shown to enhance the expression of cytotoxic cytokines .
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2.5383 20.6745 1.0000 Alpha-tocopherol treatment of the mice given the CCl4 also reduced the proteinNF-kappa B binding to levels approaching those found in normal mice .
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6.8932 30.8142 20.1151 In vitro treatment of a monocyte/macrophage cell line with CCl4 led to enhanced NF-kappa B binding and an increase in RNAtumor necrosis factor-alpha ( TNF-alpha ) messenger RNA levels .
4.1579 30.8923 10.5971 In vitro treatment of a monocyte/macrophage cell line with CCl4 led to enhanced NF-kappa B binding and an increase in proteintumor necrosis factor-alpha ( TNF-alpha ) messenger RNA levels .
1.9705 20.5686 0.9999 In vitro treatment of a monocyte/macrophage cell line with CCl4 led to enhanced proteinNF-kappa B binding and an increase in tumor necrosis factor-alpha ( TNF-alpha ) messenger RNA levels .
0.9662 1.0000 0.9975 In vitro treatment of a monocyte/macrophage cell line with CCl4 led to enhanced NF-kappa B binding and an increase in tumor necrosis factor-alpha ( proteinTNF-alpha ) messenger RNA levels .
4.1247 20.9651 10.9269 In vitro treatment of a cell_linemonocyte/macrophage cell line with CCl4 led to enhanced NF-kappa B binding and an increase in tumor necrosis factor-alpha ( TNF-alpha ) messenger RNA levels .
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2.5003 20.8194 1.0000 Liver specimens taken from patients with acute fulminant hepatitis had markedly increased proteinNF-kappa B binding activity in comparison with the binding of normal livers .
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2.4942 20.7733 1.0000 These data demonstrate that abolishing acute hepatic injury with alpha-tocopherol , a free radical scavenger , also eliminated increased proteinNF-kappa B binding .
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2.4408 20.0656 1.0000 It is tempting to speculate that enhanced proteinNF-kappa B expression caused by free radical production/oxidative stress may modulate liver injury , perhaps through an effect on cytotoxic cytokine synthesis .
2.4143 20.6712 1.0000 It is tempting to speculate that enhanced NF-kappa B expression caused by free radical production/oxidative stress may modulate liver injury , perhaps through an effect on proteincytotoxic cytokine synthesis .
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3.5783 20.4025 10.5094 Immunosuppression by glucocorticoids : inhibition of NF-kappa B activity through induction of proteinI kappa B synthesis [see comments]
2.2130 20.1331 1.0000 Immunosuppression by glucocorticoids : inhibition of proteinNF-kappa B activity through induction of I kappa B synthesis [see comments]
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3.6646 30.2431 10.6952 They inhibit synthesis of almost all known cytokines and of several proteincell surface molecules required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B ( NF-kappa B ) activation in mice and cultured cells .
3.0384 40.9296 20.6782 They inhibit synthesis of almost all known cytokines and of several cell surface molecules required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of proteinnuclear factor kappa B ( NF-kappa B ) activation in mice and cultured cells .
1.7133 10.9891 1.0000 They inhibit synthesis of almost all known cytokines and of several cell surface molecules required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B ( proteinNF-kappa B ) activation in mice and cultured cells .
1.6576 10.3066 1.0000 They inhibit synthesis of almost all known proteincytokines and of several cell surface molecules required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B ( NF-kappa B ) activation in mice and cultured cells .
1.4944 30.2870 0.9995 They inhibit synthesis of almost all known cytokines and of several cell surface molecules required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B ( NF-kappa B ) activation in mice and cell_linecultured cells .
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2.1113 10.3880 10.5215 This inhibition is mediated by induction of the I kappa B alpha inhibitory protein, which traps activated NF-kappa B in proteininactive cytoplasmic complexes .
0.6929 0.9994 1.0000 This inhibition is mediated by induction of the I kappa B alpha inhibitory protein, which traps activated proteinNF-kappa B in inactive cytoplasmic complexes .
2.8887 10.4456 10.6562 This inhibition is mediated by induction of the proteinI kappa B alpha inhibitory protein, which traps activated NF-kappa B in inactive cytoplasmic complexes .
This inhibition is mediated by induction of the proteinI kappa B alpha inhibitory protein, which traps activated NF-kappa B in inactive cytoplasmic complexes .
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1.7606 10.2092 1.0000 Because proteinNF-kappa B activates many immunoregulatory genes in response to pro-inflammatory stimuli, the inhibition of its activity can be a major component of the anti-inflammatory activity of glucocorticoids .
1.6550 10.6203 1.0000 Because NF-kappa B activates many DNAimmunoregulatory genes in response to pro-inflammatory stimuli, the inhibition of its activity can be a major component of the anti-inflammatory activity of glucocorticoids .
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4.0496 20.5068 10.6286 Transcriptional repression of the interleukin-2 gene by vitamin D3 : direct inhibition of NFATp/AP-1 complex formation by a proteinnuclear hormone receptor .
2.0923 20.5156 1.0000 Transcriptional repression of the interleukin-2 gene by vitamin D3 : direct inhibition of proteinNFATp/AP-1 complex formation by a nuclear hormone receptor .
2.0053 20.5518 1.0000 Transcriptional repression of the DNAinterleukin-2 gene by vitamin D3 : direct inhibition of NFATp/AP-1 complex formation by a nuclear hormone receptor .
1.7716 20.4318 0.9824 Transcriptional repression of the proteininterleukin-2 gene by vitamin D3 : direct inhibition of NFATp/AP-1 complex formation by a nuclear hormone receptor .
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3.5142 20.6943 10.8893 T- lymphocyte proliferation is suppressed by 1,25-dihydroxyvitamin D3 [ 1,25(OH)2D3 ], the active metabolite of vitamin D3 , and is associated with a decrease in interleukin 2 (IL-2) , gamma interferon , and proteingranulocyte-macrophage colony-stimulating factor mRNA levels .
1.9703 20.5191 0.9996 T- lymphocyte proliferation is suppressed by 1,25-dihydroxyvitamin D3 [ 1,25(OH)2D3 ], the active metabolite of vitamin D3 , and is associated with a decrease in interleukin 2 (IL-2) , gamma interferon , and RNAgranulocyte-macrophage colony-stimulating factor mRNA levels .
1.4286 10.6589 0.9992 T- lymphocyte proliferation is suppressed by 1,25-dihydroxyvitamin D3 [ 1,25(OH)2D3 ], the active metabolite of vitamin D3 , and is associated with a decrease in proteininterleukin 2 (IL-2) , gamma interferon , and granulocyte-macrophage colony-stimulating factor mRNA levels .
0.9207 0.9999 0.9996 cell_typeT- lymphocyte proliferation is suppressed by 1,25-dihydroxyvitamin D3 [ 1,25(OH)2D3 ], the active metabolite of vitamin D3 , and is associated with a decrease in interleukin 2 (IL-2) , gamma interferon , and granulocyte-macrophage colony-stimulating factor mRNA levels .
0.6904 1.0000 0.9657 cell_typeT- lymphocyte proliferation is suppressed by 1,25-dihydroxyvitamin D3 [ 1,25(OH)2D3 ], the active metabolite of vitamin D3 , and is associated with a decrease in interleukin 2 (IL-2) , gamma interferon , and granulocyte-macrophage colony-stimulating factor mRNA levels .
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3.7695 20.7367 10.6957 We report here that 1,25(OH)2D3 -mediated repression in Jurkat cells is cycloheximide resistant , suggesting that it is a direct transcriptional repressive effect on IL-2 expression by the proteinvitamin D3 receptor ( VDR ).
2.3777 20.3263 0.9999 We report here that 1,25(OH)2D3 -mediated repression in cell_lineJurkat cells is cycloheximide resistant , suggesting that it is a direct transcriptional repressive effect on IL-2 expression by the vitamin D3 receptor ( VDR ).
1.5991 10.8098 1.0000 We report here that 1,25(OH)2D3 -mediated repression in Jurkat cells is cycloheximide resistant , suggesting that it is a direct transcriptional repressive effect on proteinIL-2 expression by the vitamin D3 receptor ( VDR ).
0.9674 1.0000 1.0000 We report here that 1,25(OH)2D3 -mediated repression in Jurkat cells is cycloheximide resistant , suggesting that it is a direct transcriptional repressive effect on IL-2 expression by the vitamin D3 receptor ( proteinVDR ).
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3.0843 10.5511 10.8371 We therefore examined vitamin D3 -mediated repression of activated IL-2 expression by cotransfecting Jurkat cells with DNAIL-2 promoter/reporter constructs and a VDR overexpression vector and by DNA binding .
2.8220 20.2306 10.0230 We therefore examined vitamin D3 -mediated repression of activated IL-2 expression by cotransfecting Jurkat cells with IL-2 promoter/reporter constructs and a DNAVDR overexpression vector and by DNA binding .
2.2520 20.0372 0.9988 We therefore examined vitamin D3 -mediated repression of activated IL-2 expression by cotransfecting Jurkat cells with IL-2 promoter/reporter constructs and a proteinVDR overexpression vector and by DNA binding .
1.5575 10.4708 1.0000 We therefore examined vitamin D3 -mediated repression of activated proteinIL-2 expression by cotransfecting Jurkat cells with IL-2 promoter/reporter constructs and a VDR overexpression vector and by DNA binding .
1.4860 10.8252 0.9997 We therefore examined vitamin D3 -mediated repression of activated IL-2 expression by cotransfecting cell_lineJurkat cells with IL-2 promoter/reporter constructs and a VDR overexpression vector and by DNA binding .
1.4485 10.8476 0.9932 We therefore examined vitamin D3 -mediated repression of activated IL-2 expression by cotransfecting Jurkat cells with proteinIL-2 promoter/reporter constructs and a VDR overexpression vector and by DNA binding .
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4.3094 20.7017 10.9142 We delineated an element conferring both DNA binding by the receptor in vitro and 1,25(OH)2D3 -mediated repression in vivo to a short 40-bp region encompassing an important DNApositive regulatory element , NF-AT-1 , which is bound by a T-cell-specific transcription factor , NFATp , as well as by AP-1 .
4.0359 20.9683 10.9782 We delineated an element conferring both DNA binding by the receptor in vitro and 1,25(OH)2D3 -mediated repression in vivo to a short 40-bp region encompassing an important positive regulatory element , NF-AT-1 , which is bound by a proteinT-cell-specific transcription factor , NFATp , as well as by AP-1 .
2.1407 20.2204 0.9999 We delineated an element conferring both DNA binding by the receptor in vitro and 1,25(OH)2D3 -mediated repression in vivo to a short DNA40-bp region encompassing an important positive regulatory element , NF-AT-1 , which is bound by a T-cell-specific transcription factor , NFATp , as well as by AP-1 .
1.5940 10.1046 1.0000 We delineated an element conferring both DNA binding by the receptor in vitro and 1,25(OH)2D3 -mediated repression in vivo to a short 40-bp region encompassing an important positive regulatory element , NF-AT-1 , which is bound by a T-cell-specific transcription factor , NFATp , as well as by proteinAP-1 .
0.9593 1.0000 1.0000 We delineated an element conferring both DNA binding by the receptor in vitro and 1,25(OH)2D3 -mediated repression in vivo to a short 40-bp region encompassing an important positive regulatory element , NF-AT-1 , which is bound by a T-cell-specific transcription factor , proteinNFATp , as well as by AP-1 .
0.9206 1.0000 1.0000 We delineated an element conferring both DNA binding by the receptor in vitro and 1,25(OH)2D3 -mediated repression in vivo to a short 40-bp region encompassing an important positive regulatory element , DNANF-AT-1 , which is bound by a T-cell-specific transcription factor , NFATp , as well as by AP-1 .
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2.1140 20.4352 0.9969 VDR DNA-binding mutants were unable to either bind to this element in vitro or repress in vivo; the proteinVDR DNA-binding domain alone, however, bound the element but also could not repress IL-2 expression .
1.7752 20.3348 10.1603 VDR DNA-binding mutants were unable to either bind to this element in vitro or repress in vivo; the proteinVDR DNA-binding domain alone, however, bound the element but also could not repress IL-2 expression .
0.9452 1.0000 0.9945 proteinVDR DNA-binding mutants were unable to either bind to this element in vitro or repress in vivo; the VDR DNA-binding domain alone, however, bound the element but also could not repress IL-2 expression .
0.8493 1.0000 1.0000 VDR DNA-binding mutants were unable to either bind to this element in vitro or repress in vivo; the VDR DNA-binding domain alone, however, bound the element but also could not repress proteinIL-2 expression .
proteinVDR DNA-binding mutants were unable to either bind to this element in vitro or repress in vivo; the VDR DNA-binding domain alone, however, bound the element but also could not repress IL-2 expression .
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1.7048 10.1434 1.0000 These results indicate that DNA binding by VDR is necessary but not sufficient to mediate proteinIL-2 repression .
1.6004 10.5601 1.0000 These results indicate that DNA binding by proteinVDR is necessary but not sufficient to mediate IL-2 repression .
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3.0612 20.5457 10.5953 By combining partially purified proteins in vitro, we observed the loss of the bound NFATp /AP-1-DNA complex upon inclusion of VDR or proteinVDR -retinoid X receptor .
2.1742 20.8185 0.9999 By combining partially purified proteins in vitro, we observed the loss of the bound proteinNFATp /AP-1-DNA complex upon inclusion of VDR or VDR -retinoid X receptor .
1.9039 20.1668 0.9987 By combining partially purified proteins in vitro, we observed the loss of the bound proteinNFATp /AP-1-DNA complex upon inclusion of VDR or VDR -retinoid X receptor .
1.5843 10.0580 0.9979 By combining partially purified proteins in vitro, we observed the loss of the bound NFATp /AP-1-DNA complex upon inclusion of VDR or proteinVDR -retinoid X receptor .
1.5734 10.0675 1.0000 By combining partially purified proteins in vitro, we observed the loss of the bound NFATp /AP-1-DNA complex upon inclusion of proteinVDR or VDR -retinoid X receptor .
By combining proteinpartially purified proteins in vitro, we observed the loss of the bound NFATp /AP-1-DNA complex upon inclusion of VDR or VDR -retinoid X receptor .
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3.7959 20.2206 10.2771 Order of addition and off-rate experiments indicate that the VDR -retinoid X receptor heterodimer blocks proteinNFATp / AP-1 complex formation and then stably associates with the NF-AT-1 element .
3.5324 20.7903 10.8719 Order of addition and off-rate experiments indicate that the proteinVDR -retinoid X receptor heterodimer blocks NFATp / AP-1 complex formation and then stably associates with the NF-AT-1 element .
2.1377 20.4995 0.9999 Order of addition and off-rate experiments indicate that the VDR -retinoid X receptor heterodimer blocks NFATp / AP-1 complex formation and then stably associates with the DNANF-AT-1 element .
1.9631 20.2499 0.9977 Order of addition and off-rate experiments indicate that the proteinVDR -retinoid X receptor heterodimer blocks NFATp / AP-1 complex formation and then stably associates with the NF-AT-1 element .
1.5811 10.5405 0.9939 Order of addition and off-rate experiments indicate that the VDR -retinoid X receptor heterodimer blocks proteinNFATp / AP-1 complex formation and then stably associates with the NF-AT-1 element .
0.9021 1.0000 0.9641 Order of addition and off-rate experiments indicate that the VDR -retinoid X receptor heterodimer blocks NFATp / proteinAP-1 complex formation and then stably associates with the NF-AT-1 element .
Order of addition and off-rate experiments indicate that the VDR -retinoid X receptor heterodimer blocks NFATp / AP-1 complex formation and then stably associates with the DNANF-AT-1 element .
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2.1529 20.0746 0.9913 This direct inhibition by a nuclear hormone receptor of transcriptional activators of the proteinIL-2 gene may provide a mechanistic explanation of how vitamin derivatives can act as potent immunosuppressive agents .
1.5898 10.7777 0.9999 This direct inhibition by a nuclear hormone receptor of proteintranscriptional activators of the IL-2 gene may provide a mechanistic explanation of how vitamin derivatives can act as potent immunosuppressive agents .
1.5529 10.5819 1.0000 This direct inhibition by a nuclear hormone receptor of transcriptional activators of the DNAIL-2 gene may provide a mechanistic explanation of how vitamin derivatives can act as potent immunosuppressive agents .
4.3545 20.6198 10.6112 This direct inhibition by a proteinnuclear hormone receptor of transcriptional activators of the IL-2 gene may provide a mechanistic explanation of how vitamin derivatives can act as potent immunosuppressive agents .
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2.3605 20.3932 0.9998 Tissue-specific regulation of the DNArabbit 15-lipoxygenase gene in erythroid cells by a transcriptional silencer .
1.4117 10.5135 0.9998 Tissue-specific regulation of the rabbit 15-lipoxygenase gene in cell_typeerythroid cells by a transcriptional silencer .
1.3455 10.6653 0.9997 Tissue-specific regulation of the rabbit 15-lipoxygenase gene in erythroid cells by a DNAtranscriptional silencer .
Tissue-specific regulation of the rabbit protein15-lipoxygenase gene in erythroid cells by a transcriptional silencer .
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4.0665 20.8460 10.7606 The 15-lipoxygenase (lox) gene is expressed in a tissue-specific manner , predominantly in erythroid cells but also in cell_typeairway epithelial cells and eosinophils .
3.2380 10.8494 10.4971 The DNA15-lipoxygenase (lox) gene is expressed in a tissue-specific manner , predominantly in erythroid cells but also in airway epithelial cells and eosinophils .
2.0262 20.7602 0.9999 The 15-lipoxygenase (lox) gene is expressed in a tissue-specific manner , predominantly in cell_typeerythroid cells but also in airway epithelial cells and eosinophils .
0.7922 0.9999 0.9999 The 15-lipoxygenase (lox) gene is expressed in a tissue-specific manner , predominantly in erythroid cells but also in airway epithelial cells and cell_typeeosinophils .
1.1740 1.0000 10.5964 The 15-lipoxygenase (lox) gene is expressed in a tissue-specific manner , predominantly in erythroid cells but also in airway cell_typeepithelial cells and eosinophils .
0.7591 1.0000 0.9966 The protein15-lipoxygenase (lox) gene is expressed in a tissue-specific manner , predominantly in erythroid cells but also in airway epithelial cells and eosinophils .
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4.2831 20.9596 10.8870 We demonstrate in this report that the 5' flanking DNA of the 15-lox gene contains sequences which down-regulate its activity in a variety of non-erythroid cell lines but not in two cell_lineerythroid cell lines .
3.7570 20.8834 10.9407 We demonstrate in this report that the 5' flanking DNA of the 15-lox gene contains sequences which down-regulate its activity in a variety of cell_linenon-erythroid cell lines but not in two erythroid cell lines .
3.6071 20.5085 10.6716 We demonstrate in this report that the DNA5' flanking DNA of the 15-lox gene contains sequences which down-regulate its activity in a variety of non-erythroid cell lines but not in two erythroid cell lines .
2.1105 20.0405 1.0000 We demonstrate in this report that the 5' flanking DNA of the DNA15-lox gene contains sequences which down-regulate its activity in a variety of non-erythroid cell lines but not in two erythroid cell lines .
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The element has characteristics of a DNAtranscriptional 'silencer' since it functions in both orientations.
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3.7925 20.4919 10.6100 The main activity of the silencer has been mapped to the first 900 bp of DNA5' flanking DNA , which contains nine binding sites for a nuclear factor present in non- erythroid cells but not in erythroid cells .
2.0923 20.7943 0.9995 The main activity of the silencer has been mapped to the first 900 bp of 5' flanking DNA , which contains nine binding sites for a nuclear factor present in non- erythroid cells but not in cell_typeerythroid cells .
1.5504 10.3935 1.0000 The main activity of the DNAsilencer has been mapped to the first 900 bp of 5' flanking DNA , which contains nine binding sites for a nuclear factor present in non- erythroid cells but not in erythroid cells .
1.4272 10.8324 0.9999 The main activity of the silencer has been mapped to the first 900 bp of 5' flanking DNA , which contains nine binding sites for a proteinnuclear factor present in non- erythroid cells but not in erythroid cells .
1.2338 1.0000 10.3206 The main activity of the silencer has been mapped to the first 900 bp of 5' flanking DNA , which contains nine binding sites for a nuclear factor present in non- cell_typeerythroid cells but not in erythroid cells .
4.2006 20.5738 10.9379 The main activity of the silencer has been mapped to the first 900 bp of 5' flanking DNA , which contains nine binding sites for a nuclear factor present in cell_typenon- erythroid cells but not in erythroid cells .
2.0474 20.1693 0.9999 The main activity of the silencer has been mapped to the first 900 bp of 5' flanking DNA , which contains nine DNAbinding sites for a nuclear factor present in non- erythroid cells but not in erythroid cells .
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3.9225 20.3544 10.6969 These binding sites have similar sequences and multiple copies of the binding sites confer tissue-specific down-regulation when attached to a DNAminimal lox promoter fragment .
2.1829 20.0900 1.0000 These binding sites have similar sequences and multiple copies of the DNAbinding sites confer tissue-specific down-regulation when attached to a minimal lox promoter fragment .
1.4919 10.3552 0.9999 These DNAbinding sites have similar sequences and multiple copies of the binding sites confer tissue-specific down-regulation when attached to a minimal lox promoter fragment .
These binding sites have similar sequences and multiple copies of the binding sites confer tissue-specific down-regulation when attached to a minimal DNAlox promoter fragment .
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2.8547 10.9763 10.1941 The DNA5' flanking DNA also contains a cluster of three binding sites for the GATA family of transcription factors .
2.0270 20.2245 0.9999 The 5' flanking DNA also contains a cluster of three binding sites for the proteinGATA family of transcription factors .
1.5851 10.7495 0.9999 The 5' flanking DNA also contains a cluster of three binding sites for the GATA family of proteintranscription factors .
The 5' flanking DNA also contains a cluster of three DNAbinding sites for the GATA family of transcription factors .
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2.1292 20.3510 0.9998 Phosphorylation of the proteintranscription factor NFATp inhibits its DNA binding activity in cyclosporin A-treated human B and T cells .
0.9725 1.0000 1.0000 Phosphorylation of the transcription factor proteinNFATp inhibits its DNA binding activity in cyclosporin A-treated human B and T cells .
Phosphorylation of the transcription factor NFATp inhibits its DNA binding activity in cyclosporin A-treated human B and cell_typeT cells .
Phosphorylation of the transcription factor NFATp inhibits its DNA binding activity in cell_linecyclosporin A-treated human B and T cells .
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0.9745 1.0000 1.0000 Cyclosporin A ( CsA ) exerts its immunosuppressive effect by inhibiting the activity of nuclear factor of activated T cells ( proteinNFAT ), thus preventing transcriptional induction of several cytokine genes.
6.5969 30.9116 20.3501 Cyclosporin A ( CsA ) exerts its immunosuppressive effect by inhibiting the activity of proteinnuclear factor of activated T cells ( NFAT ), thus preventing transcriptional induction of several cytokine genes.
Cyclosporin A ( CsA ) exerts its immunosuppressive effect by inhibiting the activity of nuclear factor of activated cell_typeT cells ( NFAT ), thus preventing transcriptional induction of several cytokine genes.
Cyclosporin A ( CsA ) exerts its immunosuppressive effect by inhibiting the activity of proteinnuclear factor of activated T cells ( NFAT ), thus preventing transcriptional induction of several cytokine genes.
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2.2290 20.8976 0.9928 This effect is thought to be largely mediated through inactivation of the phosphatase calcineurin , which in turn inhibits translocation of an proteinNFAT component to the nucleus.
0.9648 1.0000 1.0000 This effect is thought to be largely mediated through inactivation of the phosphatase proteincalcineurin , which in turn inhibits translocation of an NFAT component to the nucleus.
2.2137 20.7841 1.0000 This effect is thought to be largely mediated through inactivation of the phosphatase calcineurin , which in turn inhibits translocation of an proteinNFAT component to the nucleus.
1.5541 10.4120 1.0000 This effect is thought to be largely mediated through inactivation of the proteinphosphatase calcineurin , which in turn inhibits translocation of an NFAT component to the nucleus.
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2.3334 20.4261 1.0000 Here we report that CsA treatment of Raji B and Jurkat T cell lines yields a phosphorylated form of NFATp that is inhibited in DNA-binding and in its ability to form an proteinNFAT complex with Fos and Jun .
1.6902 10.4970 1.0000 Here we report that CsA treatment of Raji B and Jurkat T cell lines yields a phosphorylated form of proteinNFATp that is inhibited in DNA-binding and in its ability to form an NFAT complex with Fos and Jun .
0.9662 1.0000 1.0000 Here we report that CsA treatment of Raji B and Jurkat T cell lines yields a phosphorylated form of NFATp that is inhibited in DNA-binding and in its ability to form an NFAT complex with Fos and proteinJun .
0.9563 1.0000 1.0000 Here we report that CsA treatment of Raji B and Jurkat T cell lines yields a phosphorylated form of NFATp that is inhibited in DNA-binding and in its ability to form an NFAT complex with proteinFos and Jun .
Here we report that CsA treatment of Raji B and cell_lineJurkat T cell lines yields a phosphorylated form of NFATp that is inhibited in DNA-binding and in its ability to form an NFAT complex with Fos and Jun .
Here we report that CsA treatment of cell_lineRaji B and Jurkat T cell lines yields a phosphorylated form of NFATp that is inhibited in DNA-binding and in its ability to form an NFAT complex with Fos and Jun .
Here we report that CsA treatment of Raji B and Jurkat cell_lineT cell lines yields a phosphorylated form of NFATp that is inhibited in DNA-binding and in its ability to form an NFAT complex with Fos and Jun .
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1.7133 10.5520 1.0000 Immunoblot analyses and metabolic labeling with [32P]orthophosphate show that CsA alters proteinNFATp migration on SDS-polyacrylamide gel electrophoresis by increasing its phosphorylation level without affecting subcellular distribution.
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1.5820 10.6458 1.0000 Dephosphorylation by in vitro treatment with calcineurin or proteinalkaline phosphatase restores NFATp DNA binding activity and its ability to reconstitute an NFAT complex with Fos and Jun proteins.
1.5352 10.9743 1.0000 Dephosphorylation by in vitro treatment with calcineurin or alkaline phosphatase restores NFATp DNA binding activity and its ability to reconstitute an proteinNFAT complex with Fos and Jun proteins.
0.8618 1.0000 1.0000 Dephosphorylation by in vitro treatment with calcineurin or alkaline phosphatase restores proteinNFATp DNA binding activity and its ability to reconstitute an NFAT complex with Fos and Jun proteins.
0.8535 0.9999 1.0000 Dephosphorylation by in vitro treatment with proteincalcineurin or alkaline phosphatase restores NFATp DNA binding activity and its ability to reconstitute an NFAT complex with Fos and Jun proteins.
0.7445 1.0000 1.0000 Dephosphorylation by in vitro treatment with calcineurin or alkaline phosphatase restores NFATp DNA binding activity and its ability to reconstitute an NFAT complex with proteinFos and Jun proteins.
Dephosphorylation by in vitro treatment with calcineurin or alkaline phosphatase restores NFATp DNA binding activity and its ability to reconstitute an NFAT complex with Fos and proteinJun proteins.
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1.6825 10.9200 1.0000 These data point to a new mechanism for CsA -sensitive regulation of proteinNFATp in which dephosphorylation is critical for DNA binding.
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0.9064 0.9997 1.0000 proteinTranscription factors as targets for oxidative signalling during lymphocyte activation .
0.6592 0.9999 0.9999 Transcription factors as targets for oxidative signalling during cell_typelymphocyte activation .
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2.5112 20.1779 1.0000 We previously have demonstrated a requirement for oxidative events during cell cycle entry in cell_typeT lymphocytes and have hypothesised that reactive oxygen species may act as intracellular signalling agents during lymphocyte activation .
0.8567 1.0000 1.0000 We previously have demonstrated a requirement for oxidative events during cell cycle entry in T lymphocytes and have hypothesised that reactive oxygen species may act as intracellular signalling agents during cell_typelymphocyte activation .
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0.8774 1.0000 1.0000 In the current study, cysteamine , an aminothiol compound with antioxidant activity , has been used to further investigate the role of oxidative signalling during cell_typelymphocyte activation .
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3.2690 20.8128 20.4403 Treatment of cell_typenormal human peripheral blood lymphocytes with cysteamine in vitro was found to inhibit proliferation in a dose-dependent manner , with essentially complete inhibition occurring at a dose of 400 microM.
Treatment of normal cell_typehuman peripheral blood lymphocytes with cysteamine in vitro was found to inhibit proliferation in a dose-dependent manner , with essentially complete inhibition occurring at a dose of 400 microM.
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2.2670 20.7812 1.0000 Taking the DNAIL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
2.2373 20.9452 0.9997 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of proteintranscription factors AP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
2.1442 20.5590 0.9998 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the proteinIL-2 mRNA.
2.0167 20.6268 0.9887 Taking the proteinIL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
0.9817 1.0000 1.0000 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors proteinAP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
0.9792 1.0000 1.0000 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , proteinNF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
0.9451 1.0000 1.0000 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , NF-AT and proteinOct1 , whose functions are required for expression of the IL-2 mRNA.
0.8572 0.9995 1.0000 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , proteinNF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
0.7585 0.9999 1.0000 Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on early gene expression during cell_typelymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
Taking the IL-2 gene as a candidate, we examined the effect of cysteamine treatment on DNAearly gene expression during lymphocyte activation , and on the activity of transcription factors AP-1 , NF-kappa B , NF-AT and Oct1 , whose functions are required for expression of the IL-2 mRNA.
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2.4545 20.1863 1.0000 Cysteamine treatment inhibited both expression of the RNAIL-2 mRNA and secretion of IL-2 into the culture medium .
1.9083 20.1912 0.9892 Cysteamine treatment inhibited both expression of the proteinIL-2 mRNA and secretion of IL-2 into the culture medium .
1.6513 10.1557 1.0000 Cysteamine treatment inhibited both expression of the IL-2 mRNA and secretion of proteinIL-2 into the culture medium .
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2.2769 20.4157 1.0000 The inhibitory effect of cysteamine may be mediated at least in part by an effect on proteintranscription factor function , as the DNA binding activities of AP-1 and NF-kappa B extracted from mitogen-stimulated cells were significantly inhibited by cysteamine treatment .
1.6331 10.8115 1.0000 The inhibitory effect of cysteamine may be mediated at least in part by an effect on transcription factor function , as the DNA binding activities of AP-1 and proteinNF-kappa B extracted from mitogen-stimulated cells were significantly inhibited by cysteamine treatment .
0.9247 0.9999 1.0000 The inhibitory effect of cysteamine may be mediated at least in part by an effect on transcription factor function , as the DNA binding activities of proteinAP-1 and NF-kappa B extracted from mitogen-stimulated cells were significantly inhibited by cysteamine treatment .
1.5462 10.6072 0.9999 The inhibitory effect of cysteamine may be mediated at least in part by an effect on transcription factor function , as the DNA binding activities of AP-1 and NF-kappa B extracted from cell_linemitogen-stimulated cells were significantly inhibited by cysteamine treatment .
The inhibitory effect of cysteamine may be mediated at least in part by an effect on transcription factor function , as the DNA binding activities of AP-1 and NF-kappa B extracted from cell_typemitogen-stimulated cells were significantly inhibited by cysteamine treatment .
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0.9356 0.9999 1.0000 Interestingly, Oct1 and proteinNF-AT DNA binding activity were not affected by cysteamine treatment, suggesting that oxidative signalling processes operate in a selective manner.
0.9247 0.9999 1.0000 Interestingly, proteinOct1 and NF-AT DNA binding activity were not affected by cysteamine treatment, suggesting that oxidative signalling processes operate in a selective manner.
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2.4608 20.4874 1.0000 The identification of proteinregulatory proteins , such as transcription factors , as molecular targets for oxidative signalling provides further evidence to implicate oxidative signalling as being intimately involved in the G0 to G1 phase transition in T lymphocytes .
2.3984 20.0053 0.9999 The identification of regulatory proteins , such as transcription factors , as molecular targets for oxidative signalling provides further evidence to implicate oxidative signalling as being intimately involved in the G0 to G1 phase transition in cell_typeT lymphocytes .
1.6330 10.9503 1.0000 The identification of regulatory proteins , such as proteintranscription factors , as molecular targets for oxidative signalling provides further evidence to implicate oxidative signalling as being intimately involved in the G0 to G1 phase transition in T lymphocytes .
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3.2782 10.9223 10.9104 Sex and age distribution of 1,25(OH)2D3 receptors in cell_typeperipheral blood mononuclear cells from normal human subjects .
1.6280 20.0700 0.9998 Sex and age distribution of protein1,25(OH)2D3 receptors in peripheral blood mononuclear cells from normal human subjects .
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0.8860 0.9999 0.9999 Specific receptors for 1,25 Dihydroxyvitamin D3 have been described in human peripheral blood mononuclear cells ( cell_typePBMC ).
5.3476 20.9149 20.0417 Specific receptors for 1,25 Dihydroxyvitamin D3 have been described in cell_typehuman peripheral blood mononuclear cells ( PBMC ).
Specific receptors for 1,25 Dihydroxyvitamin D3 have been described in human cell_typeperipheral blood mononuclear cells ( PBMC ).
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0.9638 1.0000 1.0000 The mean dissociation constant ( Kd ) was similar in both sexes (1.35 +/- 0.70 x 10(-10) M in males, 1.13 +/- 0.66 x 10(-10) M in females), but the concentration of binding sites (Nmax) was significantly lower in females (2.32 +/- 0.92 fmol/10(7) cell_typePBMC vs 4.43 +/- 1.38 fmol/10(7) PBMC in males ; p = 0.0001).
0.9636 1.0000 1.0000 The mean dissociation constant ( Kd ) was similar in both sexes (1.35 +/- 0.70 x 10(-10) M in males, 1.13 +/- 0.66 x 10(-10) M in females), but the concentration of binding sites (Nmax) was significantly lower in females (2.32 +/- 0.92 fmol/10(7) PBMC vs 4.43 +/- 1.38 fmol/10(7) cell_typePBMC in males ; p = 0.0001).
1.9468 20.4507 1.0000 The mean dissociation constant ( Kd ) was similar in both sexes (1.35 +/- 0.70 x 10(-10) M in males, 1.13 +/- 0.66 x 10(-10) M in females), but the concentration of proteinbinding sites (Nmax) was significantly lower in females (2.32 +/- 0.92 fmol/10(7) PBMC vs 4.43 +/- 1.38 fmol/10(7) PBMC in males ; p = 0.0001).
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2.1438 20.8108 0.9675 Further studies are needed to elucidate if this sex difference in cell_typePBMC receptors for 1.25 Dihydroxyvitamin D3 is of any pathophysiological relevance .
2.0382 20.9774 1.0000 Further studies are needed to elucidate if this sex difference in proteinPBMC receptors for 1.25 Dihydroxyvitamin D3 is of any pathophysiological relevance .
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2.0991 20.1658 0.9998 Expression of Id2 and Id3 mRNA in cell_typehuman lymphocytes .
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2.6029 0.9967 20.1493 proteinHelix-loop-helix ( HLH ) transcription factors are involved in cellular growth and differentiation .
0.6953 1.0000 0.9803 proteinHelix-loop-helix ( HLH ) transcription factors are involved in cellular growth and differentiation .
0.7171 0.9561 0.9996 Helix-loop-helix ( HLH ) proteintranscription factors are involved in cellular growth and differentiation .
Helix-loop-helix ( proteinHLH ) transcription factors are involved in cellular growth and differentiation .
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1.8836 30.4539 10.5898 The Id ( inhibitor of DNA binding and differentiation ) HLH proteins , in a dominantly negative fashion, regulate transcriptional activities of proteinbasic HLH proteins .
4.0332 10.7269 20.8770 The proteinId ( inhibitor of DNA binding and differentiation ) HLH proteins , in a dominantly negative fashion, regulate transcriptional activities of basic HLH proteins .
The Id ( inhibitor of DNA binding and differentiation ) proteinHLH proteins , in a dominantly negative fashion, regulate transcriptional activities of basic HLH proteins .
The proteinId ( inhibitor of DNA binding and differentiation ) HLH proteins , in a dominantly negative fashion, regulate transcriptional activities of basic HLH proteins .
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4.0613 20.5019 10.8108 We examined by northern hybridization the expression of Id2 and Id3 mRNA in cell_linehuman leukemia/lymphoma lines and patient samples , as well as resting and activated normal human lymphocytes from peripheral blood ( PBL ).
0.9319 1.0000 1.0000 We examined by northern hybridization the expression of Id2 and Id3 mRNA in human leukemia/lymphoma lines and patient samples , as well as resting and activated normal human lymphocytes from peripheral blood ( cell_typePBL ).
2.5418 10.9985 10.7868 We examined by northern hybridization the expression of Id2 and Id3 mRNA in human leukemia/lymphoma lines and patient samples , as well as resting and activated cell_typenormal human lymphocytes from peripheral blood ( PBL ).
We examined by northern hybridization the expression of Id2 and Id3 mRNA in human leukemia/lymphoma lines and patient samples , as well as resting and cell_lineactivated normal human lymphocytes from peripheral blood ( PBL ).
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1.7690 10.5590 0.9999 The RNAId2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
1.7046 10.8674 1.0000 The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and RNAId3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
1.2787 10.5098 0.9995 The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 cell_lineB-cell lines .
1.2603 10.6136 0.9998 The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 cell_lineB-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
0.7496 1.0000 0.9999 The Id2 mRNA was abundantly expressed in 5/12 cell_lineT-cell and 3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
The proteinId2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and proteinId3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
The Id2 mRNA was abundantly expressed in 5/12 T-cell and cell_line3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
The Id2 mRNA was abundantly expressed in cell_line5/12 T-cell and 3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and 3/4 B-cell lines .
The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and Id3 mRNA was detected in 4/12 T-cell and cell_line3/4 B-cell lines .
The Id2 mRNA was abundantly expressed in 5/12 T-cell and 3/4 B-cell lines , and Id3 mRNA was detected in cell_line4/12 T-cell and 3/4 B-cell lines .
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1.7272 10.4548 1.0000 Interestingly, Id2 , but not proteinId3 , mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , MT-2 , S-LB1 ) and type II ( Mo ) .
0.9417 0.9999 1.0000 Interestingly, Id2 , but not Id3 , mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , MT-2 , cell_lineS-LB1 ) and type II ( Mo ) .
0.9268 1.0000 1.0000 Interestingly, Id2 , but not Id3 , mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , cell_lineMT-2 , S-LB1 ) and type II ( Mo ) .
0.8899 1.0000 1.0000 Interestingly, proteinId2 , but not Id3 , mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , MT-2 , S-LB1 ) and type II ( Mo ) .
0.8531 1.0000 1.0000 Interestingly, Id2 , but not Id3 , mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( cell_lineATL-1k , MT-2 , S-LB1 ) and type II ( Mo ) .
0.6122 0.9999 1.0000 Interestingly, Id2 , but not Id3 , mRNA was strongly expressed in 4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , MT-2 , S-LB1 ) and type II ( cell_lineMo ) .
1.4904 10.7977 0.9999 Interestingly, Id2 , but not Id3 , mRNA was strongly expressed in 4/5 cell_lineT-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , MT-2 , S-LB1 ) and type II ( Mo ) .
Interestingly, Id2 , but not Id3 , mRNA was strongly expressed in cell_line4/5 T-cell lines infected with human T-cell leukemia virus type I ( HTLV-I ) ( ATL-1k , MT-2 , S-LB1 ) and type II ( Mo ) .
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1.6360 10.8867 0.9999 Another unexpected finding was that T-cell leukemias and cell_lineT-cell lines often expressed either Id2 or Id3 mRNA .
Another unexpected finding was that T-cell leukemias and T-cell lines often expressed either Id2 or RNAId3 mRNA .
Another unexpected finding was that T-cell leukemias and T-cell lines often expressed either proteinId2 or Id3 mRNA .
Another unexpected finding was that T-cell leukemias and T-cell lines often expressed either Id2 or proteinId3 mRNA .
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2.4804 20.3051 1.0000 In addition, resting PBL constitutively expressed prominent levels of RNAId2 mRNA , but not Id3 mRNA .
2.3909 20.4427 0.9999 In addition, resting PBL constitutively expressed prominent levels of Id2 mRNA , but not RNAId3 mRNA .
1.9857 20.0464 0.9999 In addition, cell_typeresting PBL constitutively expressed prominent levels of Id2 mRNA , but not Id3 mRNA .
0.8882 1.0000 1.0000 In addition, resting cell_typePBL constitutively expressed prominent levels of Id2 mRNA , but not Id3 mRNA .
In addition, resting PBL constitutively expressed prominent levels of Id2 mRNA , but not proteinId3 mRNA .
In addition, resting PBL constitutively expressed prominent levels of proteinId2 mRNA , but not Id3 mRNA .
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1.7498 10.2542 1.0000 Upon PHA -stimulation , proteinId2 expression decreased and Id3 levels increased with biphasic kinetics.
0.9500 1.0000 1.0000 Upon proteinPHA -stimulation , Id2 expression decreased and Id3 levels increased with biphasic kinetics.
0.8721 1.0000 1.0000 Upon PHA -stimulation , Id2 expression decreased and proteinId3 levels increased with biphasic kinetics.
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2.5293 20.9994 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of RNAId2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
2.4787 20.6126 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of RNAId3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
2.0622 20.5647 0.9917 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of proteinId2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
2.0484 20.7889 0.9926 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of proteinId3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
1.7115 10.5580 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of RNAId2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
1.6442 10.4208 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or RNAId3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
1.5089 10.5725 0.9875 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or proteinId3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
1.4733 10.6859 0.9955 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of proteinId2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
1.2382 20.0407 0.9883 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no proteinId3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
0.9578 1.0000 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal cell_typePBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
0.8310 1.0000 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either proteinId2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
0.7925 0.9974 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no RNAId3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
0.7565 1.0000 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of proteinId2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
3.7708 30.1342 10.7495 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) cell_typenon-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
0.8989 1.0000 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) cell_typeT-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
0.8509 1.0000 1.0000 Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but cell_typeB-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related genes is disparate.
Taken together, our studies revealed three unexpected findings which require further analysis: (1) expression of Id2 mRNA is often associated with lymphocytic transformation by HTLV-I or -II; (2) T-cells usually express either Id2 or Id3 mRNA , but B-cells often express both simultaneously; (3) non-dividing, normal PBL express high levels of Id2 and no Id3 mRNA ; and with the onset of cellular proliferation, levels of Id2 mRNA decrease while levels of Id3 mRNA increase, suggesting that regulation of expression of these closely related DNAgenes is disparate.
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2.8438 10.6069 10.5315 Salicylates inhibit lipopolysaccharide -induced transcriptional activation of the tissue factor gene in cell_typehuman monocytic cells .
3.4799 20.2212 10.7385 Salicylates inhibit lipopolysaccharide -induced transcriptional activation of the DNAtissue factor gene in human monocytic cells .
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3.7944 20.4685 10.8958 Binding of proteinplasma Factor VII/VIIa to the tissue factor (TF) receptor initiates the coagulation protease cascades .
3.6030 20.2862 10.9471 Binding of plasma Factor VII/VIIa to the proteintissue factor (TF) receptor initiates the coagulation protease cascades .
1.2676 10.2626 0.9999 Binding of plasma Factor VII/VIIa to the tissue factor (TF) receptor initiates the proteincoagulation protease cascades .
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2.2370 20.0849 0.9999 TF expression by cell_typecirculating monocytes is associated with thrombotic and inflammatory complications in a variety of diseases.
0.9654 1.0000 1.0000 proteinTF expression by circulating monocytes is associated with thrombotic and inflammatory complications in a variety of diseases.
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4.1807 20.6604 10.8568 Transcriptional activation of the human TF gene in monocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of c-Rel/p65 heterodimers to a DNAkappa B site in the TF promoter .
3.7072 20.8779 10.7887 Transcriptional activation of the DNAhuman TF gene in monocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of c-Rel/p65 heterodimers to a kappa B site in the TF promoter .
2.1465 20.6372 0.9998 Transcriptional activation of the human TF gene in monocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of c-Rel/p65 heterodimers to a kappa B site in the DNATF promoter .
2.0760 20.6853 1.0000 Transcriptional activation of the human TF gene in monocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of proteinc-Rel/p65 heterodimers to a kappa B site in the TF promoter .
1.5091 10.2965 0.9998 Transcriptional activation of the human TF gene in cell_typemonocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of c-Rel/p65 heterodimers to a kappa B site in the TF promoter .
1.9765 20.8954 0.9893 Transcriptional activation of the human TF gene in monocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of c-Rel/p65 heterodimers to a kappa B site in the proteinTF promoter .
1.5618 20.8958 0.9679 Transcriptional activation of the human TF gene in monocytic cells exposed to bacterial lipopolysaccharide ( LPS ) is mediated by binding of proteinc-Rel/p65 heterodimers to a kappa B site in the TF promoter .
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3.2180 10.9845 10.9405 Here, we report that a family of anti-inflammatory agents , known as the salicylates, inhibited LPS induction of TF activity and TF gene transcription in human monocytes and cell_linemonocytic THP-1 cells at clinically relevant doses.
1.5258 10.9609 1.0000 Here, we report that a family of anti-inflammatory agents , known as the salicylates, inhibited LPS induction of TF activity and DNATF gene transcription in human monocytes and monocytic THP-1 cells at clinically relevant doses.
1.4954 10.6366 0.9998 Here, we report that a family of anti-inflammatory agents , known as the salicylates, inhibited LPS induction of TF activity and TF gene transcription in cell_typehuman monocytes and monocytic THP-1 cells at clinically relevant doses.
1.0305 10.9186 0.9770 Here, we report that a family of anti-inflammatory agents , known as the salicylates, inhibited LPS induction of TF activity and proteinTF gene transcription in human monocytes and monocytic THP-1 cells at clinically relevant doses.
0.8875 1.0000 1.0000 Here, we report that a family of anti-inflammatory agents , known as the salicylates, inhibited LPS induction of proteinTF activity and TF gene transcription in human monocytes and monocytic THP-1 cells at clinically relevant doses.
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3.8824 20.7110 10.8138 Furthermore, sodium salicylate blocked the LPS -induced proteolytic degradation of proteinI kappa B alpha , which prevented the nuclear translocation of c-Rel/p65 heterodimers .
2.1244 20.7404 0.9999 Furthermore, sodium salicylate blocked the LPS -induced proteolytic degradation of I kappa B alpha , which prevented the nuclear translocation of proteinc-Rel/p65 heterodimers .
1.9878 20.8863 0.9755 Furthermore, sodium salicylate blocked the LPS -induced proteolytic degradation of I kappa B alpha , which prevented the nuclear translocation of proteinc-Rel/p65 heterodimers .
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2.3839 20.6799 1.0000 In contrast, two other nonsteroidal anti-inflammatory drugs , ibuprofen and indomethacin , did not inhibit LPS induction of the DNATF gene .
2.0734 20.6191 0.9843 In contrast, two other nonsteroidal anti-inflammatory drugs , ibuprofen and indomethacin , did not inhibit LPS induction of the proteinTF gene .
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2.2282 20.2720 0.9999 These results indicated that salicylates inhibited LPS induction of TF gene transcription in monocytic cells by preventing nuclear translocation of proteinc-Rel/p65 heterodimers .
1.4952 10.7686 1.0000 These results indicated that salicylates inhibited LPS induction of DNATF gene transcription in monocytic cells by preventing nuclear translocation of c-Rel/p65 heterodimers .
1.4503 10.7525 0.9999 These results indicated that salicylates inhibited LPS induction of TF gene transcription in cell_typemonocytic cells by preventing nuclear translocation of c-Rel/p65 heterodimers .
2.1182 20.6670 0.9858 These results indicated that salicylates inhibited LPS induction of TF gene transcription in monocytic cells by preventing nuclear translocation of proteinc-Rel/p65 heterodimers .
1.2623 10.7930 0.9905 These results indicated that salicylates inhibited LPS induction of proteinTF gene transcription in monocytic cells by preventing nuclear translocation of c-Rel/p65 heterodimers .
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1.5038 20.2149 1.0000 The clinical benefits of salicylates in the treatment of several diseases, including atherosclerosis and rheumatoid arthritis , may be related to their ability to reduce DNAmonocyte gene expression .
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0.9762 1.0000 1.0000 Activation of the signal transducer and transcription ( proteinSTAT ) signaling pathway in a primary T cell response .
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0.7269 0.9999 1.0000 Critical role for proteinIL-6 .
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0.9645 1.0000 1.0000 The T cell activation is initiated by interaction of specific Ags with proteinTCR , followed by activation of intracellular biochemical events leading to activation of several genes.
0.6369 1.0000 1.0000 The T cell activation is initiated by interaction of specific proteinAgs with TCR , followed by activation of intracellular biochemical events leading to activation of several genes.
2.3472 20.5678 1.0000 The T cell activation is initiated by interaction of proteinspecific Ags with TCR , followed by activation of intracellular biochemical events leading to activation of several genes.
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1.1723 20.1428 0.9998 The activation of signal transducer and activator of transcription (STAT) proteins in a primary TCR -mediated activation of cell_typeT cells have been explored.
0.8806 1.0000 1.0000 The activation of signal transducer and activator of transcription (STAT) proteins in a primary proteinTCR -mediated activation of T cells have been explored.
4.8142 30.8059 20.3787 The activation of proteinsignal transducer and activator of transcription (STAT) proteins in a primary TCR -mediated activation of T cells have been explored.
1.5330 20.3148 0.9997 The activation of signal transducer and activator of transcription (STAT) proteins in a proteinprimary TCR -mediated activation of T cells have been explored.
The activation of signal transducer and activator of proteintranscription (STAT) proteins in a primary TCR -mediated activation of T cells have been explored.
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4.6234 10.5746 20.3673 In cell_typepurified human peripheral blood T cells , nuclear STAT proteins were activated approximately 3 h after activation by cross-linked anti-CD3 Abs .
1.9339 30.9173 10.1488 In purified human peripheral blood T cells , nuclear STAT proteins were activated approximately 3 h after activation by proteincross-linked anti-CD3 Abs .
1.8989 20.7543 0.9999 In purified human peripheral blood T cells , nuclear proteinSTAT proteins were activated approximately 3 h after activation by cross-linked anti-CD3 Abs .
In purified human peripheral blood T cells , proteinnuclear STAT proteins were activated approximately 3 h after activation by cross-linked anti-CD3 Abs .
In purified human peripheral blood T cells , nuclear STAT proteins were activated approximately 3 h after activation by cross-linked proteinanti-CD3 Abs .
In purified human peripheral blood cell_typeT cells , nuclear STAT proteins were activated approximately 3 h after activation by cross-linked anti-CD3 Abs .
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1.5944 10.8835 1.0000 These STAT proteins were detected by using the DNAIFN-gamma-activated sequence ( GAS ) and related oligonucleotides as probes in electrophoretic mobility shift assay .
1.5513 10.1822 1.0000 These proteinSTAT proteins were detected by using the IFN-gamma-activated sequence ( GAS ) and related oligonucleotides as probes in electrophoretic mobility shift assay .
0.9503 1.0000 1.0000 These STAT proteins were detected by using the IFN-gamma-activated sequence ( DNAGAS ) and related oligonucleotides as probes in electrophoretic mobility shift assay .
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1.6393 10.2165 1.0000 Analysis of the nuclear extracts with anti-STAT Abs indicated that they contained proteinSTAT-3 and additional proteins crossreactive with the STAT family .
1.5448 10.9848 1.0000 Analysis of the nuclear extracts with proteinanti-STAT Abs indicated that they contained STAT-3 and additional proteins crossreactive with the STAT family .
1.4508 10.8084 0.9999 Analysis of the nuclear extracts with anti-STAT Abs indicated that they contained STAT-3 and additional proteins crossreactive with the proteinSTAT family .
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2.9991 30.1343 0.9993 The induction of proteinSTAT activity was inhibited completely by pretreatment with either cycloheximide or cyclosporin A , thus indicating that the induction was due to a secondary factor produced by the activated T cells .
2.3582 20.8233 1.0000 The induction of STAT activity was inhibited completely by pretreatment with either cycloheximide or cyclosporin A , thus indicating that the induction was due to a proteinsecondary factor produced by the activated T cells .
3.8173 20.8271 10.9785 The induction of STAT activity was inhibited completely by pretreatment with either cycloheximide or cyclosporin A , thus indicating that the induction was due to a secondary factor produced by the cell_typeactivated T cells .
1.5947 20.7997 1.0000 The induction of proteinSTAT activity was inhibited completely by pretreatment with either cycloheximide or cyclosporin A , thus indicating that the induction was due to a secondary factor produced by the activated T cells .
The induction of STAT activity was inhibited completely by pretreatment with either cycloheximide or cyclosporin A , thus indicating that the induction was due to a secondary factor produced by the activated cell_typeT cells .
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2.2377 20.7347 1.0000 As neutralizing anti- IL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of proteinSTAT proteins in a primary T cell response .
2.1881 20.4767 1.0000 As neutralizing anti- IL-6 Abs effectively down-regulated the early induction of proteinSTAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
1.9088 20.5662 0.9883 As neutralizing anti- proteinIL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
1.6375 10.3368 1.0000 As neutralizing anti- IL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added proteinIL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
0.9106 1.0000 1.0000 As neutralizing anti- IL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that proteinIL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
0.9030 1.0000 1.0000 As neutralizing anti- IL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to proteinTCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
2.3776 20.8154 10.2336 As neutralizing proteinanti- IL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
As proteinneutralizing anti- IL-6 Abs effectively down-regulated the early induction of STAT proteins and as exogenously added IL-6 rapidly activated DNA binding similar to TCR -mediated bindings , it can be concluded that IL-6 is the factor responsible for the activation of STAT proteins in a primary T cell response .
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3.7110 20.9621 10.4043 The normal cell cycle activation program is exploited during the infection of cell_typequiescent B lymphocytes by Epstein-Barr virus .
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0.8895 0.9988 0.9999 cell_typeB lymphocytes in the peripheral circulation are maintained in a non-proliferative state .
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4.1336 20.8383 10.3523 Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus ( EBV ) results in continual proliferation and the outgrowth of cell_lineimmortal cell lines .
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4.5440 30.0598 10.8571 Because it is not clear at which point in cell cycle the peripheral B lymphocytes are arrested, we characterized the expression of several DNAcell cycle-associated genes in quiescent and stimulated cells .
3.8527 20.7763 10.9256 Because it is not clear at which point in cell cycle the cell_typeperipheral B lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells .
Because it is not clear at which point in cell cycle the peripheral cell_typeB lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells .
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1.9607 10.6162 10.1019 We show that the expression of four DNAcell genes , cdc-2 , cyclin E , CD23 , and cyclin D2 , are up-regulated approximately 100-fold as a result of EBV -mediated immortalization .
1.8327 10.0851 1.0000 We show that the expression of four cell genes , DNAcdc-2 , cyclin E , CD23 , and cyclin D2 , are up-regulated approximately 100-fold as a result of EBV -mediated immortalization .
1.5999 10.3470 1.0000 We show that the expression of four cell genes , cdc-2 , DNAcyclin E , CD23 , and cyclin D2 , are up-regulated approximately 100-fold as a result of EBV -mediated immortalization .
1.5845 10.5712 1.0000 We show that the expression of four cell genes , cdc-2 , cyclin E , CD23 , and DNAcyclin D2 , are up-regulated approximately 100-fold as a result of EBV -mediated immortalization .
0.9457 1.0000 1.0000 We show that the expression of four cell genes , cdc-2 , cyclin E , DNACD23 , and cyclin D2 , are up-regulated approximately 100-fold as a result of EBV -mediated immortalization .
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3.8454 20.5096 10.7665 Transient stimulation of cell_typequiescent B lymphocytes with either a cocktail of anti-CD40 , anti-IgM , and IL4 , or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation .
1.7572 10.2938 1.0000 Transient stimulation of quiescent B lymphocytes with either a cocktail of proteinanti-CD40 , anti-IgM , and IL4 , or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation .
1.7025 10.4775 1.0000 Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40 , anti-IgM , and proteinIL4 , or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation .
0.9450 1.0000 1.0000 Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40 , proteinanti-IgM , and IL4 , or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation .
0.8746 0.9998 1.0000 Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40 , anti-IgM , and IL4 , or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of cell_typeB-lymphocyte cell cycle activation .
Transient stimulation of quiescent cell_typeB lymphocytes with either a cocktail of anti-CD40 , anti-IgM , and IL4 , or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation .
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5.0060 20.8956 20.3990 Expression of the chemokine receptor BLR2/EBI1 is specifically transactivated by proteinEpstein-Barr virus nuclear antigen 2 .
1.6822 20.6357 0.9990 Expression of the proteinchemokine receptor BLR2/EBI1 is specifically transactivated by Epstein-Barr virus nuclear antigen 2 .
0.9408 0.9999 1.0000 Expression of the chemokine receptor proteinBLR2/EBI1 is specifically transactivated by Epstein-Barr virus nuclear antigen 2 .
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3.9270 20.8910 10.9981 In our attempt to identify chemokine receptors that are related to proteinBurkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in activated lymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a seven transmembrane receptor termed BLR2 .
3.5636 20.9890 10.9068 In our attempt to identify chemokine receptors that are related to Burkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in activated lymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a proteinseven transmembrane receptor termed BLR2 .
1.3856 10.9662 0.9999 In our attempt to identify proteinchemokine receptors that are related to Burkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in activated lymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a seven transmembrane receptor termed BLR2 .
1.2758 10.8568 0.9997 In our attempt to identify chemokine receptors that are related to Burkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in cell_typeactivated lymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a seven transmembrane receptor termed BLR2 .
0.9708 1.0000 1.0000 In our attempt to identify chemokine receptors that are related to Burkitt's lymphoma receptor 1 ( proteinBLR1 ) and are expressed in activated lymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a seven transmembrane receptor termed BLR2 .
0.8920 1.0000 1.0000 In our attempt to identify chemokine receptors that are related to Burkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in activated lymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a seven transmembrane receptor termed proteinBLR2 .
1.5561 10.0642 1.0000 In our attempt to identify chemokine receptors that are related to Burkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in activated lymphocytes we used RT-PCR resulting in the isolation of a DNAcDNA encoding a seven transmembrane receptor termed BLR2 .
0.8692 1.0000 0.9999 In our attempt to identify chemokine receptors that are related to Burkitt's lymphoma receptor 1 ( BLR1 ) and are expressed in activated cell_typelymphocytes we used RT-PCR resulting in the isolation of a cDNA encoding a seven transmembrane receptor termed BLR2 .
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3.9324 20.9386 10.7696 The protein shows significant sequence similarities to the family of proteinG-protein coupled chemokine receptors and turned out to be identical to the recently described receptor EBI1 .
2.0449 20.0693 0.9999 The protein shows significant sequence similarities to the family of G-protein coupled chemokine receptors and turned out to be identical to the recently described proteinreceptor EBI1 .
0.8441 0.9995 0.9999 The protein shows significant sequence similarities to the family of G-protein coupled proteinchemokine receptors and turned out to be identical to the recently described receptor EBI1 .
0.5139 1.0000 1.0000 The protein shows significant sequence similarities to the family of G-protein coupled chemokine receptors and turned out to be identical to the recently described receptor proteinEBI1 .
The protein shows significant sequence similarities to the family of proteinG-protein coupled chemokine receptors and turned out to be identical to the recently described receptor EBI1 .
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2.4028 20.0940 1.0000 Northern blot analysis revealed that RNABLR2 mRNA could be highly stimulated in mitogen- and anti-CD3- treated peripheral blood lymphocytes .
1.9950 20.1325 0.9954 Northern blot analysis revealed that proteinBLR2 mRNA could be highly stimulated in mitogen- and anti-CD3- treated peripheral blood lymphocytes .
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6.8860 30.4520 20.1967 BLR2 -specific mRNA could be detected in all cell_lineEpstein-Barr virus positive B cell lines .
0.9582 1.0000 0.9998 proteinBLR2 -specific mRNA could be detected in all Epstein-Barr virus positive B cell lines .
0.5415 0.8507 0.9998 RNABLR2 -specific mRNA could be detected in all Epstein-Barr virus positive B cell lines .
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6.2510 30.9578 20.4714 We show that transcription of the BLR2 gene could be specifically induced in cell_lineEpstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of viral and cellular genes in immortalized B cells .
5.0533 30.4028 20.0640 We show that transcription of the BLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of proteinEpstein-Barr virus nuclear antigen 2 , a key regulator of viral and cellular genes in immortalized B cells .
1.8348 20.9459 1.0000 We show that transcription of the DNABLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of viral and cellular genes in immortalized B cells .
1.7519 20.9117 0.9927 We show that transcription of the proteinBLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of viral and cellular genes in immortalized B cells .
1.3475 0.9832 10.0267 We show that transcription of the BLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of viral and cellular genes in cell_lineimmortalized B cells .
We show that transcription of the BLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of DNAviral and cellular genes in immortalized B cells .
We show that transcription of the BLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of viral and DNAcellular genes in immortalized B cells .
We show that transcription of the BLR2 gene could be specifically induced in Epstein-Barr virus negative BL 41 cells via estrogen-mediated activation of Epstein-Barr virus nuclear antigen 2 , a key regulator of DNAviral and cellular genes in immortalized B cells .
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2.2778 20.1925 1.0000 Our data suggest an involvement of proteinBLR2 in the regulation of migration in activated lymphocytes and in viral pathogenesis .
0.9309 1.0000 1.0000 Our data suggest an involvement of BLR2 in the regulation of migration in activated cell_typelymphocytes and in viral pathogenesis .
Our data suggest an involvement of BLR2 in the regulation of migration in cell_typeactivated lymphocytes and in viral pathogenesis .
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3.6591 20.3568 10.7893 A central role for a single c-Myb binding site in a DNAthymic locus control region .
3.3024 20.4082 10.7641 A central role for a single DNAc-Myb binding site in a thymic locus control region .
A central role for a DNAsingle c-Myb binding site in a thymic locus control region .
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3.4542 20.7922 10.6094 Locus control regions ( LCRs ) are powerful assemblies of cis elements that organize the actions of proteincell-type-specific trans-acting factors .
1.9441 20.2241 0.9999 Locus control regions ( LCRs ) are powerful assemblies of DNAcis elements that organize the actions of cell-type-specific trans-acting factors .
1.4606 0.9980 10.6391 DNALocus control regions ( LCRs ) are powerful assemblies of cis elements that organize the actions of cell-type-specific trans-acting factors .
0.9501 1.0000 1.0000 Locus control regions ( DNALCRs ) are powerful assemblies of cis elements that organize the actions of cell-type-specific trans-acting factors .
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6.7054 30.2481 20.5713 A 2.3-kb LCR in the DNAhuman adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
3.9108 20.9596 10.9876 A 2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a DNA200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
1.4533 10.0240 1.0000 A 2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in cell_typethymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
1.3405 10.6535 1.0000 A 2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within DNAchromatin .
2.7063 20.1810 10.5779 A 2.3-kb LCR in the proteinhuman adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
1.6652 20.6754 0.9998 A 2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended DNAflanking sequences that facilitate activation from within chromatin .
1.2897 10.6066 0.9991 A DNA2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
0.5606 1.0000 0.9998 A 2.3-kb DNALCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
A 2.3-kb LCR in the DNAhuman adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
A protein2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron , which controls expression in thymocytes , is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin .
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2.6757 10.8519 10.7748 Prior analyses have demonstrated that the enhancer contains a DNA28-bp core region and local adjacent augmentative cis elements .
4.7697 20.9982 20.7290 Prior analyses have demonstrated that the enhancer contains a 28-bp core region and DNAlocal adjacent augmentative cis elements .
Prior analyses have demonstrated that the DNAenhancer contains a 28-bp core region and local adjacent augmentative cis elements .
Prior analyses have demonstrated that the enhancer contains a 28-bp core region and local adjacent augmentative DNAcis elements .
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3.7082 20.5312 10.4767 We now show that the core contains a single critical DNAc-Myb binding site .
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3.8681 30.1247 10.5759 In both transiently cotransfected human cells and stable chromatin-integrated yeast cells , c-Myb strongly transactivated reporter constructs that contained DNApolymerized core sequences .
3.7249 20.2250 10.8508 In both cell_linetransiently cotransfected human cells and stable chromatin-integrated yeast cells , c-Myb strongly transactivated reporter constructs that contained polymerized core sequences .
1.2831 0.9988 10.7122 In both transiently cotransfected human cells and stable cell_linechromatin-integrated yeast cells , c-Myb strongly transactivated reporter constructs that contained polymerized core sequences .
0.9419 1.0000 1.0000 In both transiently cotransfected human cells and stable chromatin-integrated yeast cells , proteinc-Myb strongly transactivated reporter constructs that contained polymerized core sequences .
In both transiently cotransfected human cells and stable chromatin-integrated yeast cells , c-Myb strongly DNAtransactivated reporter constructs that contained polymerized core sequences .
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2.2250 20.7382 0.9999 c-Myb protein was strongly evident in cell_typeT lymphoblasts in which the enhancer was active and was localized within discrete nuclear structures .
0.9321 1.0000 0.9927 proteinc-Myb protein was strongly evident in T lymphoblasts in which the enhancer was active and was localized within discrete nuclear structures .
0.8839 0.9980 0.9999 proteinc-Myb protein was strongly evident in T lymphoblasts in which the enhancer was active and was localized within discrete nuclear structures .
c-Myb protein was strongly evident in T lymphoblasts in which the DNAenhancer was active and was localized within discrete nuclear structures .
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1.7325 10.5309 1.0000 Fetal murine thymus exhibited a striking concordance of endogenous DNAc-myb expression with that of mouse ADA and human ADA LCR -directed transgene expression .
1.1603 10.4022 0.8702 Fetal murine thymus exhibited a striking concordance of endogenous c-myb expression with that of mouse ADA and DNAhuman ADA LCR -directed transgene expression .
2.2224 20.1592 0.9999 Fetal murine thymus exhibited a striking concordance of endogenous c-myb expression with that of proteinmouse ADA and human ADA LCR -directed transgene expression .
Fetal murine thymus exhibited a striking concordance of endogenous c-myb expression with that of DNAmouse ADA and human ADA LCR -directed transgene expression .
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2.1476 20.4186 1.0000 Point mutation of the DNAc-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in transgenic thymocytes .
0.8692 1.0000 1.0000 Point mutation of the c-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and DNALCR activity in transgenic thymocytes .
2.1998 20.1046 0.9999 Point mutation of the c-Myb site within the intact DNA2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in transgenic thymocytes .
1.4101 10.6075 0.9997 Point mutation of the c-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in cell_typetransgenic thymocytes .
0.5403 1.0000 1.0000 Point mutation of the c-Myb site within the intact 2.3-kb LCR severely attenuated DNAenhancer activity in transfections and LCR activity in transgenic thymocytes .
0.5219 1.0000 1.0000 Point mutation of the c-Myb site within the intact 2.3-kb DNALCR severely attenuated enhancer activity in transfections and LCR activity in transgenic thymocytes .
Point mutation of the c-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in transgenic cell_typethymocytes .
Point mutation of the c-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in cell_linetransgenic thymocytes .
Point mutation of the c-Myb site within the intact protein2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in transgenic thymocytes .
Point mutation of the proteinc-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in transgenic thymocytes .
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2.0061 20.3557 0.9999 Within the context of a DNAcomplex enhancer and LCR , c-Myb can act as an organizer of thymocyte-specific gene expression via a single binding site.
1.6521 10.1307 1.0000 Within the context of a complex enhancer and DNALCR , c-Myb can act as an organizer of thymocyte-specific gene expression via a single binding site.
1.5212 20.2415 0.9999 Within the context of a complex enhancer and LCR , c-Myb can act as an organizer of DNAthymocyte-specific gene expression via a single binding site.
0.8096 1.0000 1.0000 Within the context of a complex enhancer and LCR , proteinc-Myb can act as an organizer of thymocyte-specific gene expression via a single binding site.
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.6267 30.8111 20.4368 A regulatory element in the DNAhuman interleukin 2 gene promoter is a binding site for the zinc finger proteins Sp1 and EGR-1 .
2.5504 20.7338 10.2510 A regulatory element in the human interleukin 2 gene promoter is a binding site for the proteinzinc finger proteins Sp1 and EGR-1 .
1.8955 20.5322 0.9999 A regulatory element in the human interleukin 2 gene promoter is a DNAbinding site for the zinc finger proteins Sp1 and EGR-1 .
1.2508 10.8091 0.9996 A DNAregulatory element in the human interleukin 2 gene promoter is a binding site for the zinc finger proteins Sp1 and EGR-1 .
0.9584 1.0000 1.0000 A regulatory element in the human interleukin 2 gene promoter is a binding site for the zinc finger proteins Sp1 and proteinEGR-1 .
0.9484 0.9999 1.0000 A regulatory element in the human interleukin 2 gene promoter is a binding site for the zinc finger proteins proteinSp1 and EGR-1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0784 30.6125 20.3909 Activation of the DNAinterleukin 2 ( IL-2 ) gene after antigen recognition is a critical event for T cell proliferation and effector function.
0.9612 1.0000 0.9926 Activation of the interleukin 2 ( proteinIL-2 ) gene after antigen recognition is a critical event for T cell proliferation and effector function.
Activation of the proteininterleukin 2 ( IL-2 ) gene after antigen recognition is a critical event for T cell proliferation and effector function.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.1415 20.4674 1.0000 Prior studies have identified several transcription factors that contribute to the activity of the DNAIL-2 promoter in stimulated T lymphocytes .
2.1351 20.2977 1.0000 Prior studies have identified several proteintranscription factors that contribute to the activity of the IL-2 promoter in stimulated T lymphocytes .
1.9443 20.4203 0.9886 Prior studies have identified several transcription factors that contribute to the activity of the proteinIL-2 promoter in stimulated T lymphocytes .
1.4947 10.6970 0.9995 Prior studies have identified several transcription factors that contribute to the activity of the IL-2 promoter in stimulated cell_typeT lymphocytes .
Prior studies have identified several transcription factors that contribute to the activity of the IL-2 promoter in cell_typestimulated T lymphocytes .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6535 20.9627 0.9998 Here we describe a novel DNAregulatory element within the IL-2 promoter located immediately upstream of the nuclear factor of activated T cell ( NFAT ) domain .
1.1499 20.5701 0.9999 Here we describe a novel regulatory element within the DNAIL-2 promoter located immediately upstream of the nuclear factor of activated T cell ( NFAT ) domain .
0.9651 1.0000 0.9609 Here we describe a novel regulatory element within the IL-2 promoter located immediately upstream of the nuclear factor of activated T cell ( proteinNFAT ) domain .
1.8720 20.7713 20.4415 Here we describe a novel regulatory element within the IL-2 promoter located immediately upstream of the proteinnuclear factor of activated T cell ( NFAT ) domain .
Here we describe a novel regulatory element within the IL-2 promoter located immediately upstream of the proteinnuclear factor of activated T cell ( NFAT ) domain .
Here we describe a novel regulatory element within the IL-2 promoter located immediately upstream of the DNAnuclear factor of activated T cell ( NFAT ) domain .
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.9189 40.2977 10.8150 This region (termed the zinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed transcription factor Sp1 and the proteininducible early growth response protein EGR-1 .
4.6469 30.9516 10.9807 This region (termed the DNAzinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed transcription factor Sp1 and the inducible early growth response protein EGR-1 .
3.9052 20.8879 10.5683 This region (termed the zinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated proteinzinc finger proteins : the constitutively expressed transcription factor Sp1 and the inducible early growth response protein EGR-1 .
0.9575 0.9998 1.0000 This region (termed the zinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed transcription factor Sp1 and the inducible early growth response protein proteinEGR-1 .
0.9500 0.9999 1.0000 This region (termed the zinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed transcription factor proteinSp1 and the inducible early growth response protein EGR-1 .
0.8966 1.0000 1.0000 This region (termed the zinc finger protein binding region ( DNAZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed transcription factor Sp1 and the inducible early growth response protein EGR-1 .
3.7645 30.9674 10.6907 This region (termed the proteinzinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed transcription factor Sp1 and the inducible early growth response protein EGR-1 .
1.9382 20.3064 0.9980 This region (termed the zinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the constitutively expressed proteintranscription factor Sp1 and the inducible early growth response protein EGR-1 .
This region (termed the zinc finger protein binding region ( ZIP )) serves as binding site for two differently regulated zinc finger proteins : the proteinconstitutively expressed transcription factor Sp1 and the inducible early growth response protein EGR-1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.7702 10.5132 10.4867 In cell_typeunstimulated cells which do not secrete IL-2 , only Sp1 binds to this region, while in stimulated IL-2 secreting cells the inducible EGR-1 protein recognizes this element.
2.1172 20.2999 10.1991 In unstimulated cells which do not secrete IL-2 , only Sp1 binds to this region, while in stimulated IL-2 secreting cells the proteininducible EGR-1 protein recognizes this element.
1.6096 10.1230 1.0000 In unstimulated cells which do not secrete IL-2 , only proteinSp1 binds to this region, while in stimulated IL-2 secreting cells the inducible EGR-1 protein recognizes this element.
1.4895 10.7694 1.0000 In unstimulated cells which do not secrete proteinIL-2 , only Sp1 binds to this region, while in stimulated IL-2 secreting cells the inducible EGR-1 protein recognizes this element.
0.9220 1.0000 0.9861 In unstimulated cells which do not secrete IL-2 , only Sp1 binds to this region, while in stimulated proteinIL-2 secreting cells the inducible EGR-1 protein recognizes this element.
In unstimulated cells which do not secrete IL-2 , only Sp1 binds to this region, while in stimulated IL-2 secreting cells the inducible proteinEGR-1 protein recognizes this element.
In unstimulated cells which do not secrete IL-2 , only Sp1 binds to this region, while in cell_linestimulated IL-2 secreting cells the inducible EGR-1 protein recognizes this element.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.7951 10.9040 10.5745 In Jurkat T cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and DNANFAT binding sites is required for maximal IL-2 promoter activity .
2.2699 10.7103 10.5038 In cell_lineJurkat T cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
2.1803 20.3005 0.9999 In Jurkat T cells , the DNAZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
2.0861 20.1740 0.9818 In Jurkat T cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal proteinIL-2 promoter activity .
2.0096 20.3037 0.9886 In Jurkat T cells , the ZIP site serves as an activator for proteinIL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
1.3914 10.9457 0.9998 In Jurkat T cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal DNAIL-2 promoter activity .
0.6978 0.9999 0.9998 In Jurkat T cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of DNAZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
2.1022 20.2078 1.0000 In Jurkat T cells , the ZIP site serves as an activator for DNAIL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
1.0543 1.0000 10.1483 In Jurkat cell_typeT cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
In Jurkat T cells , the ZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and proteinNFAT binding sites is required for maximal IL-2 promoter activity .
In Jurkat T cells , the DNAZIP site serves as an activator for IL-2 gene expression , and a combination of ZIP and NFAT binding sites is required for maximal IL-2 promoter activity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2240 20.0892 0.9999 These results suggest a critical role of the DNAZIP site for IL-2 promoter activity .
1.5334 10.9183 0.9997 These results suggest a critical role of the ZIP site for DNAIL-2 promoter activity .
1.2083 10.9946 0.9723 These results suggest a critical role of the ZIP site for proteinIL-2 promoter activity .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.6742 10.9956 10.8374 Activation of the HIV-1 enhancer by the proteinLEF-1 HMG protein on nucleosome-assembled DNA in vitro.
1.9840 20.1565 0.9999 Activation of the DNAHIV-1 enhancer by the LEF-1 HMG protein on nucleosome-assembled DNA in vitro.
1.3837 10.8139 0.9998 Activation of the HIV-1 enhancer by the LEF-1 HMG protein on DNAnucleosome-assembled DNA in vitro.
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.5400 30.4989 20.8852 Lymphoid enhancer-binding factor 1 ( LEF-1 ) is a regulatory high mobility group (HMG) protein that activates the DNAT cell receptor alpha ( TCR alpha ) enhancer in a context-restricted manner in T cells .
5.5159 30.6595 20.8509 Lymphoid enhancer-binding factor 1 ( LEF-1 ) is a proteinregulatory high mobility group (HMG) protein that activates the T cell receptor alpha ( TCR alpha ) enhancer in a context-restricted manner in T cells .
1.6294 30.0238 0.9988 Lymphoid enhancer-binding factor 1 ( LEF-1 ) is a regulatory high mobility group (HMG) protein that activates the T cell receptor alpha ( TCR alpha ) enhancer in a context-restricted manner in cell_typeT cells .
0.9639 1.0000 1.0000 Lymphoid enhancer-binding factor 1 ( proteinLEF-1 ) is a regulatory high mobility group (HMG) protein that activates the T cell receptor alpha ( TCR alpha ) enhancer in a context-restricted manner in T cells .
0.7440 0.9923 0.9983 proteinLymphoid enhancer-binding factor 1 ( LEF-1 ) is a regulatory high mobility group (HMG) protein that activates the T cell receptor alpha ( TCR alpha ) enhancer in a context-restricted manner in T cells .
0.7038 1.0000 0.9501 Lymphoid enhancer-binding factor 1 ( LEF-1 ) is a regulatory high mobility group (HMG) protein that activates the T cell receptor alpha ( proteinTCR alpha ) enhancer in a context-restricted manner in T cells .
Lymphoid enhancer-binding factor 1 ( LEF-1 ) is a regulatory high mobility group (HMG) protein that activates the proteinT cell receptor alpha ( TCR alpha ) enhancer in a context-restricted manner in T cells .
Cls_Score Left_Reg_Score Right_Reg_Score Text
6.2932 30.8653 30.1155 In this paper we demonstrate that the distal region of the DNAhuman immunodeficiency virus-1 ( HIV-1 ) enhancer , which contains DNA-binding sites for LEF-1 and Ets-1, also provides a functional context for activation by LEF-1 .
2.0369 20.2106 1.0000 In this paper we demonstrate that the distal region of the human immunodeficiency virus-1 ( HIV-1 ) enhancer , which contains DNA-binding sites for LEF-1 and Ets-1, also provides a functional context for activation by proteinLEF-1 .
1.9558 20.8194 0.9999 In this paper we demonstrate that the distal region of the human immunodeficiency virus-1 ( HIV-1 ) enhancer , which contains DNADNA-binding sites for LEF-1 and Ets-1, also provides a functional context for activation by LEF-1 .
0.9178 1.0000 1.0000 In this paper we demonstrate that the distal region of the human immunodeficiency virus-1 ( HIV-1 ) enhancer , which contains DNA-binding sites for proteinLEF-1 and Ets-1, also provides a functional context for activation by LEF-1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.0854 20.7479 10.0021 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat T cells , and that LEF-1 /GAL4 can activate a DNAGAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
2.9989 20.7435 10.9116 First, we show that mutations in the DNALEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat T cells , and that LEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
2.9000 10.8534 10.5064 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in cell_lineJurkat T cells , and that LEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
2.3187 20.0647 0.9968 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat T cells , and that proteinLEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
2.1267 20.0323 0.9970 First, we show that mutations in the proteinLEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat T cells , and that LEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
1.4954 10.2466 1.0000 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat T cells , and that proteinLEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
1.3745 10.9691 0.9998 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the DNAHIV-1 enhancer in Jurkat T cells , and that LEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
0.6531 0.9999 0.9997 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat T cells , and that LEF-1 /GAL4 can activate a GAL4-substituted DNAHIV-1 enhancer 80- to 100-fold in vivo.
0.6798 1.0000 0.9999 First, we show that mutations in the LEF-1 -binding site inhibit the activity of multimerized copies of the HIV-1 enhancer in Jurkat cell_typeT cells , and that LEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
First, we show that mutations in the LEF-1 -binding site inhibit the activity of DNAmultimerized copies of the HIV-1 enhancer in Jurkat T cells , and that LEF-1 /GAL4 can activate a GAL4-substituted HIV-1 enhancer 80- to 100-fold in vivo.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4330 10.9123 0.9999 Second, recombinant LEF-1 is shown to activate HIV-1 transcription on DNAchromatin-assembled DNA in vitro.
1.3288 10.2907 0.9999 Second, proteinrecombinant LEF-1 is shown to activate HIV-1 transcription on chromatin-assembled DNA in vitro.
0.9679 1.0000 1.0000 Second, recombinant proteinLEF-1 is shown to activate HIV-1 transcription on chromatin-assembled DNA in vitro.
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1260 30.0157 1.0000 By using a nucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into chromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with LEF-1 (or LEF-1 and Ets-1 ) supplemented with fractions containing the proteinpromoter-binding protein , Sp1 .
1.7407 10.8646 1.0000 By using a nucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into DNAchromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with LEF-1 (or LEF-1 and Ets-1 ) supplemented with fractions containing the promoter-binding protein , Sp1 .
1.7038 10.7801 1.0000 By using a nucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into chromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with proteinLEF-1 (or LEF-1 and Ets-1 ) supplemented with fractions containing the promoter-binding protein , Sp1 .
0.9681 1.0000 1.0000 By using a nucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into chromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with LEF-1 (or LEF-1 and proteinEts-1 ) supplemented with fractions containing the promoter-binding protein , Sp1 .
0.9362 1.0000 1.0000 By using a nucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into chromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with LEF-1 (or LEF-1 and Ets-1 ) supplemented with fractions containing the promoter-binding protein , proteinSp1 .
0.9073 1.0000 1.0000 By using a nucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into chromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with LEF-1 (or proteinLEF-1 and Ets-1 ) supplemented with fractions containing the promoter-binding protein , Sp1 .
By using a proteinnucleosome -assembly system derived from Drosophila embryos , we find that the packaging of DNA into chromatin in vitro strongly represses HIV-1 transcription and that repression can be counteracted efficiently by preincubation of the DNA with LEF-1 (or LEF-1 and Ets-1 ) supplemented with fractions containing the promoter-binding protein , Sp1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5776 10.4858 0.9999 Addition of TFE-3 , which binds to an DNAE-box motif upstream of the LEF-1 and Ets-1 sites , further augments transcription in this system.
1.7506 10.3513 1.0000 Addition of DNATFE-3 , which binds to an E-box motif upstream of the LEF-1 and Ets-1 sites , further augments transcription in this system.
1.7060 10.7948 10.0920 Addition of TFE-3 , which binds to an E-box motif upstream of the DNALEF-1 and Ets-1 sites , further augments transcription in this system.
Addition of proteinTFE-3 , which binds to an E-box motif upstream of the LEF-1 and Ets-1 sites , further augments transcription in this system.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2723 20.5869 1.0000 Individually or collectively, none of the three proteinenhancer-binding proteins ( LEF-1 , Ets-1 , and TFE-3 ) could activate transcription in the absence of Sp1 .
1.7283 10.5349 1.0000 Individually or collectively, none of the three enhancer-binding proteins ( LEF-1 , Ets-1 , and proteinTFE-3 ) could activate transcription in the absence of Sp1 .
1.4859 10.7647 1.0000 Individually or collectively, none of the three enhancer-binding proteins ( LEF-1 , Ets-1 , and TFE-3 ) could activate transcription in the absence of proteinSp1 .
0.9597 1.0000 1.0000 Individually or collectively, none of the three enhancer-binding proteins ( LEF-1 , proteinEts-1 , and TFE-3 ) could activate transcription in the absence of Sp1 .
0.8964 1.0000 1.0000 Individually or collectively, none of the three enhancer-binding proteins ( proteinLEF-1 , Ets-1 , and TFE-3 ) could activate transcription in the absence of Sp1 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2920 20.5095 1.0000 A truncation mutant of LEF-1 ( HMG-88 ), which contains the HMG box but lacks the trans-activation domain , did not activate transcription from DNAnucleosomal DNA , indicating that bending of DNA by the HMG domain is not sufficient to activate transcription in vitro.
2.2884 20.1493 1.0000 A truncation mutant of LEF-1 ( HMG-88 ), which contains the HMG box but lacks the trans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNA by the proteinHMG domain is not sufficient to activate transcription in vitro.
2.2623 20.6853 1.0000 A truncation mutant of LEF-1 ( HMG-88 ), which contains the HMG box but lacks the proteintrans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNA by the HMG domain is not sufficient to activate transcription in vitro.
2.2574 20.8356 1.0000 A truncation mutant of LEF-1 ( HMG-88 ), which contains the proteinHMG box but lacks the trans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNA by the HMG domain is not sufficient to activate transcription in vitro.
1.6743 10.9652 1.0000 A truncation mutant of proteinLEF-1 ( HMG-88 ), which contains the HMG box but lacks the trans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNA by the HMG domain is not sufficient to activate transcription in vitro.
0.9843 1.0000 1.0000 A truncation mutant of LEF-1 ( proteinHMG-88 ), which contains the HMG box but lacks the trans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNA by the HMG domain is not sufficient to activate transcription in vitro.
0.8011 0.9999 1.0000 A truncation mutant of LEF-1 ( HMG-88 ), which contains the HMG box but lacks the trans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNADNA by the HMG domain is not sufficient to activate transcription in vitro.
A proteintruncation mutant of LEF-1 ( HMG-88 ), which contains the HMG box but lacks the trans-activation domain , did not activate transcription from nucleosomal DNA , indicating that bending of DNA by the HMG domain is not sufficient to activate transcription in vitro.
Cls_Score Left_Reg_Score Right_Reg_Score Text
2.2528 20.5003 1.0000 We conclude that transcription activation by LEF-1 in vitro is a chromatin -dependent process that requires a functional proteintrans-activation domain in addition to the HMG domain .
2.2092 20.6120 0.9999 We conclude that transcription activation by LEF-1 in vitro is a chromatin -dependent process that requires a functional trans-activation domain in addition to the proteinHMG domain .
1.7928 10.3885 1.0000 We conclude that transcription activation by LEF-1 in vitro is a DNAchromatin -dependent process that requires a functional trans-activation domain in addition to the HMG domain .
1.5607 10.9290 1.0000 We conclude that transcription activation by proteinLEF-1 in vitro is a chromatin -dependent process that requires a functional trans-activation domain in addition to the HMG domain .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.1638 10.7101 10.4425 HIV-1 envelope glycoproteins induce activation of activated protein-1 in cell_typeCD4+ T cells [published erratum appears in J Biol Chem 1995 Dec 1;270(48):29038]
1.5530 0.9992 10.9213 proteinHIV-1 envelope glycoproteins induce activation of activated protein-1 in CD4+ T cells [published erratum appears in J Biol Chem 1995 Dec 1;270(48):29038]
2.0297 20.0519 0.9999 HIV-1 envelope glycoproteins induce activation of proteinactivated protein-1 in CD4+ T cells [published erratum appears in J Biol Chem 1995 Dec 1;270(48):29038]
HIV-1 envelope glycoproteins induce activation of activated proteinprotein-1 in CD4+ T cells [published erratum appears in J Biol Chem 1995 Dec 1;270(48):29038]
HIV-1 envelope glycoproteins induce activation of activated protein-1 in CD4+ cell_typeT cells [published erratum appears in J Biol Chem 1995 Dec 1;270(48):29038]
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.3621 30.9415 20.9033 Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing cell_lineCD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
2.4062 20.9111 10.7102 Activation of cell_typeCD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
2.2185 20.4816 1.0000 Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , proteingp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
1.3911 30.8684 0.9998 Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that proteinnative envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
1.2121 20.5719 0.9994 Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and cell_typepurified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
0.9752 1.0000 1.0000 Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( proteinAP-1 ).
0.8021 0.9982 0.9999 Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, proteinactivated protein-1 ( AP-1 ).
Activation of CD4 positive cell_typeT cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified T cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of proteintranscription factor, activated protein-1 ( AP-1 ).
Activation of CD4 positive T cells is a primary requirement for human immunodeficiency virus ( HIV ) entry , efficient HIV replication , and progression to AIDS , Utilizing CD4 positive T cell lines and purified cell_typeT cells from normal individuals , we have demonstrated that native envelope glycoproteins of HIV , gp 160 , can induce activation of transcription factor, activated protein-1 ( AP-1 ).
Cls_Score Left_Reg_Score Right_Reg_Score Text
5.1633 20.8109 10.8802 The stimulatory effects of gp160 are mediated through the CD4 molecule , since treatment of gp160 with soluble CD4-IgG abrogates its activity, and cell_lineCD4 negative T cell lines fail to be stimulated with gp160 .
2.0283 20.1787 1.0000 The stimulatory effects of gp160 are mediated through the proteinCD4 molecule , since treatment of gp160 with soluble CD4-IgG abrogates its activity, and CD4 negative T cell lines fail to be stimulated with gp160 .
1.4259 10.5039 1.0000 The stimulatory effects of gp160 are mediated through the CD4 molecule , since treatment of gp160 with soluble proteinCD4-IgG abrogates its activity, and CD4 negative T cell lines fail to be stimulated with gp160 .
1.7048 20.5483 0.9870 The stimulatory effects of gp160 are mediated through the proteinCD4 molecule , since treatment of gp160 with soluble CD4-IgG abrogates its activity, and CD4 negative T cell lines fail to be stimulated with gp160 .
0.5270 1.0000 0.9970 The stimulatory effects of gp160 are mediated through the CD4 molecule , since treatment of gp160 with soluble CD4-IgG abrogates its activity, and proteinCD4 negative T cell lines fail to be stimulated with gp160 .
The stimulatory effects of proteingp160 are mediated through the CD4 molecule , since treatment of gp160 with soluble CD4-IgG abrogates its activity, and CD4 negative T cell lines fail to be stimulated with gp160 .
The stimulatory effects of gp160 are mediated through the CD4 molecule , since treatment of proteingp160 with soluble CD4-IgG abrogates its activity, and CD4 negative T cell lines fail to be stimulated with gp160 .
The stimulatory effects of gp160 are mediated through the CD4 molecule , since treatment of gp160 with soluble CD4-IgG abrogates its activity, and CD4 negative T cell lines fail to be stimulated with proteingp160 .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.5724 10.8356 1.0000 Immunoprecipitation of the gp 160 -induced nuclear extracts with polyclonal antibodies to Fos and Jun proteins indicates that proteinAP-1 complex is comprised of members of these family of proteins.
1.5068 10.3420 1.0000 Immunoprecipitation of the gp 160 -induced nuclear extracts with proteinpolyclonal antibodies to Fos and Jun proteins indicates that AP-1 complex is comprised of members of these family of proteins.
0.9182 1.0000 1.0000 Immunoprecipitation of the gp 160 -induced nuclear extracts with polyclonal antibodies to proteinFos and Jun proteins indicates that AP-1 complex is comprised of members of these family of proteins.
0.7788 0.9966 1.0000 Immunoprecipitation of the gp 160 -induced nuclear extracts with polyclonal antibodies to Fos and proteinJun proteins indicates that AP-1 complex is comprised of members of these family of proteins.
1.6964 10.0328 0.9961 Immunoprecipitation of the gp 160 -induced nuclear extracts with polyclonal antibodies to Fos and proteinJun proteins indicates that AP-1 complex is comprised of members of these family of proteins.
Immunoprecipitation of the gp 160 -induced nuclear extracts with polyclonal antibodies to Fos and Jun proteins indicates that proteinAP-1 complex is comprised of members of these family of proteins.
Immunoprecipitation of the proteingp 160 -induced nuclear extracts with polyclonal antibodies to Fos and Jun proteins indicates that AP-1 complex is comprised of members of these family of proteins.
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.6156 10.6211 0.9971 The proteingp160 -induced AP-1 complex is dependent upon protein tyrosine phosphorylation and is protein synthesis-independent .
0.6883 1.0000 0.8826 The gp160 -induced proteinAP-1 complex is dependent upon protein tyrosine phosphorylation and is protein synthesis-independent .
0.7992 0.9982 0.9999 The gp160 -induced proteinAP-1 complex is dependent upon protein tyrosine phosphorylation and is protein synthesis-independent .
The proteingp160 -induced AP-1 complex is dependent upon protein tyrosine phosphorylation and is protein synthesis-independent .
Cls_Score Left_Reg_Score Right_Reg_Score Text
3.9039 20.5912 10.4237 This stimulation can also be abolished by inhibitors of proteinprotein kinase C , but it is unaffected by calcium channel blocker or cyclosporine A .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0553 20.9077 10.5643 This gp160 treatment adversely affects the functional capabilities of T cells : pre-treatment of cell_typeCD4+ T cells with gp160 for 4 h at 37 degrees C inhibited anti-CD3 -induced interleukin-2 secretion .
2.2531 20.4856 0.9999 This gp160 treatment adversely affects the functional capabilities of cell_typeT cells : pre-treatment of CD4+ T cells with gp160 for 4 h at 37 degrees C inhibited anti-CD3 -induced interleukin-2 secretion .
1.6944 10.1147 1.0000 This gp160 treatment adversely affects the functional capabilities of T cells : pre-treatment of CD4+ T cells with gp160 for 4 h at 37 degrees C inhibited proteinanti-CD3 -induced interleukin-2 secretion .
0.8591 1.0000 1.0000 This gp160 treatment adversely affects the functional capabilities of T cells : pre-treatment of CD4+ T cells with gp160 for 4 h at 37 degrees C inhibited anti-CD3 -induced proteininterleukin-2 secretion .
This proteingp160 treatment adversely affects the functional capabilities of T cells : pre-treatment of CD4+ T cells with gp160 for 4 h at 37 degrees C inhibited anti-CD3 -induced interleukin-2 secretion .
This gp160 treatment adversely affects the functional capabilities of T cells : pre-treatment of CD4+ cell_typeT cells with gp160 for 4 h at 37 degrees C inhibited anti-CD3 -induced interleukin-2 secretion .
This gp160 treatment adversely affects the functional capabilities of T cells : pre-treatment of CD4+ T cells with proteingp160 for 4 h at 37 degrees C inhibited anti-CD3 -induced interleukin-2 secretion .
Cls_Score Left_Reg_Score Right_Reg_Score Text
1.4434 10.9082 0.9999 Effects similar to gp160 were seen with proteinanti-CD4 mAb .
Effects similar to proteingp160 were seen with anti-CD4 mAb .
Cls_Score Left_Reg_Score Right_Reg_Score Text
4.0922 20.6968 10.9713 The aberrant activation of AP-1 by gp160 in cell_typeCD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
3.9749 20.4109 10.9826 The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and proteingranulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
1.4592 10.7929 0.9902 The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing proteinAP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
1.4511 10.3430 1.0000 The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting proteininterleukin-2 secretion .
0.8722 0.9999 1.0000 The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of proteincytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
0.8683 0.9999 1.0000 The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. proteininterleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
0.8389 0.9999 1.0000 The aberrant activation of proteinAP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
1.0014 10.6083 1.0000 The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing proteinAP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
0.6178 1.0000 0.9957 The aberrant activation of AP-1 by gp160 in proteinCD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to cell_typeT cell unresponsiveness by inhibiting interleukin-2 secretion .
The aberrant activation of AP-1 by proteingp160 in CD4 positive T cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
The aberrant activation of AP-1 by gp160 in CD4 positive T cells could result in up-regulation of cytokines containing DNAAP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .
The aberrant activation of AP-1 by gp160 in CD4 positive cell_typeT cells could result in up-regulation of cytokines containing AP-1 sites , e.g. interleukin-3 and granulocyte macrophage colony-stimulating factor , and concurrently lead to T cell unresponsiveness by inhibiting interleukin-2 secretion .